Download MBBS Ophthalmology PPT 21 Chronic Conjunctivitis And Trachoma Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Ophthalmology PPT 21 Chronic Conjunctivitis And Trachoma Lecture Notes

Chronic Conjunctivitis and Trachoma

VERNAL KERATOCONJUNCTIVITIS (VKC) OR

SPRING CATARRH

It is a recurrent, bilateral, interstitial, self-limiting,
al ergic inflammation of the conjunctiva having a
periodic seasonal incidence.

An atopic al ergic disorder in many cases, in

which IgE-mediated mechanisms play an

important role.




Predisposing factors

1. Age and sex. 4-20 years; more common in boys.

2. Season. More common in summer; hence the

name spring catarrh looks a misnomer.

Recently it is being label ed as 'Warm weather

conjunctivitis'.

3. Climate. More prevalent in tropics, less in

temperate zones and almost non-existent in cold

climate.

Clinical picture
Symptoms. Spring catarrh is characterised by

marked burning and itching sensation, mild to

severe photophobia, lacrimation, stringy (ropy)

discharge and heaviness of lids.

Signs of vernal keratoconjunctivitis can be

described in fol owing three clinical forms:

1. Palpebral form.
2. Bulbar form.
3. Mixed form.


1. Palpebral form. Usually upper tarsal

conjunctivaof both eyes is involved.

The typical lesion is characterized by the

presence of hard, flat topped, papillae arranged

in a 'cobble-stone' or 'pavement stone', fashion.

In severe cases, papillae may hypertrophy to

produce cauliflower like excrescences of 'giant

papillae'. Conjunctival changes are associated

with white ropy discharge.

2. Bulbar form.

(i) dusky red triangular

congestion of bulbar

conjunctiva in palpebral area;


(ii) gelatinous thickened

accumulation of tissue around

the limbus; and


(ii ) presence of discrete whitish

raised dots along the limbus

(Tranta's spots)
Vernal keratopathy. Corneal involvement in VKC

may be primary or secondary due to extension of limbal

lesions.

1. Punctate epithelial keratitis involving upper cornea is

usual y associated with palpebral form of disease.

2.Ulcerative vernal keratitis (shield ulceration) presents as a

shal ow transverse ulcer in upper part of cornea.

3. Vernal corneal plaques

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
Treatment

A. Local therapy
1. Topical steroids.
2. Mast cel stabilizers such as sodium

cromoglycate (2%) drops.

3. Topical antihistaminics.
4. Topical cyclosporine drops.

B. Systemic antihistamincs

C. General measures include :
Dark goggles to prevent photophobia.
Cold compresses and ice packs have soothing effects.
Change of place from hot to cold area is recommended
for recalcitrant cases.
D. Treatment of vernal keratopathy
Punctate epithelial keratitis requires no extra

treatment except that instillation of steroids should be

increased.

Severe shield ulcer resistant to medical therapy may

need surgical treatment in the form of debridment,

superficial keratectomy, excimer laser therapeutic

kerateotomy as well as amniotic membrane

transplantation to enhance re-epithelialization.

CHLAMYDIAL CONJUNCTIVITIS
Like viruses they are obligate intracellular and

filterable

Like bacteria they contain both DNA and RNA,

divide by binary fission and are sensitive to

antibiotics.

Combinedly form the PLT group (Psittacosis,

Lymphogranuloma venereum andTrachomatis

group).
Species C. trachomatis C. lymphogranulomatis C.

psittacosis

Jones' classification.
Class 1 : Blinding trachoma refers to

hyperendemic trachoma caused by serotypes

A,B, Ba and C of Chlamydia trachomatis

associated with secondary bacterial infection.

Class 2 : Non-blinding trachoma by serotypes A,

B, Ba, and C; but is usual y not associated with

secondary bacterial infections.

Class 3: Paratrachoma. It refers to 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 chlamydial ophthalmia

neonatorum.
TRACHOMA

The word 'trachoma' (Greek word)stands for

'rough' which describes the surface appearance of

the conjunctiva in chronic trachoma.

A type of chronic keratoconjunctivitis, primarily

affecting the superficial epithelium of conjunctiva

and cornea simultaneously.

A. Causative organism: Chlamydia trachomatis
The organism is epitheliotropic and produces

intracytoplasmic inclusion bodies called H.P. bodies

(Halberstaedter Prowazeke bodies).

11 serotypes of chlamydia
Microimmunofluorescence techniques
B. Predisposing factors.
1. Age. 3. Race (Jews). 5. Socioeconomic status.
2. Sex. 4. Climate. 6. Environmental factors
C. Source of infection: Conjunctival discharge of the affected

person

D. Modes of infection:
1. Direct spread (Air, Water)
2. Vector transmission (Flies)
3. Material transfer (Towel, handkerchief, surma rods)

Clinical profile of trachoma
Incubation period of trachoma varies from 5-22 days.

Onset of disease is usually insidious (subacute),

however, rarely it may present in acute form.
In the absence of Secondary infection, a pure trachoma is
mild and symptomless.
But, mostly the picture is complicated by secondary infection
In the early stages it is clinically indistinguishable from the
bacterial conjunctivitis and the term 'trachoma dubium'
(doubtful trachoma) is sometimes used for this stage.


A. Conjunctival signs
1. Congestion of upper tarsal and forniceal conjunctiva.
2. Conjunctival follicles: Like boiled sagograins, commonly on

upper tarsal plate 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 formed due to scattered aggregation of lymphocytes

and 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.
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.

4.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
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.

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.
McCal an's classification
Stage I (Incipient trachoma or stage of infiltration).
It is characterized by hyperaemia of 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 (Cicatrising trachoma 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 1987 (FISTO):
1. TF: Trachomatous inflammation-follicular: At least

five or more follicles (each 0.5 mm or more in diameter)

must be present on the upper tarsal conjunctiva.

Further, the deep tarsal vessels should be visible through the

follicles and papillae.

2. TI : Trachomatous inflammation intense: 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.

4. TT: Trachomatous trichiasis. TT is labelled when at least one eyelash

rubs the eyeball.

5. CO: Corneal opacity: easily visible corneal opacity is present over the

pupil.
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: corneal ulcer

Diagnosis
A. The clinical diagnosis of trachoma is made from its

typical signs; at least two sets of signs should be present out

of the following:

1. Conjunctival follicles and papillae
2. Pannus progressive or regressive
3. Epithelial keratitis near superior limbus
4. Signs of cicatrisation or its sequelae
B. Laboratory diagnosis.
1. Conjunctival cytology. Giemsa stained smears
showing a predominantly polymorphonuclear
reaction with presence of plasma cells and Leber
cells is suggestive of trachoma.
2. Detection of inclusion bodies in conjunctival
smear may be possible by Giemsa stain, iodine stain or

immunofluorescent staining, specially in cases with active

trachoma.

3. Enzyme-linked immunosorbent assay (ELISA) for
chlamydial antigens.
4. Polymerase chain reaction (PCR) is also useful.
5. Isolation of chlamydia is possible by yolk-sac
inoculation method and tissue culture technique.
Standard single-passage McCoy cell culture requires at least 3

days.
6. Serotyping of TRIC agents is done by detecting
specific antibodies using microimmunofluorescence
(micro-IF) method.
Direct monoclonal fluorescent antibody microscopy of
conjunctival smear is rapid and inexpensive.

Differential diagnosis
1. Trachoma with follicular hypertrophy must be
differentiated from acute adenoviral follicular
conjunctivitis (epidemic keratoconjunctivitis).

2. Trachoma with predominant papillary
hypertrophy needs to be differentiated from palpebral form of

spring catarrh
Management
A. Treatment of active trachoma
1. Topical therapy regimes
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.

The continuous treatment for active trachoma should be followed

by an intermittent treatment especially in endemic or

hyperendemic area.

2. Systemic therapy regimes. Tetracycline or erythromycin 250 mg

orally, four times a day for 3-4 weeks
or
doxycycline 100 mg orally twice daily for 3-4 weeks or single

dose of 1 gm azithromycin has also been reported to be equally

effective in treating trachoma.
B. Treatment of trachoma sequelae
C. Prophylaxis
1. Hygienic measures.
2. Early treatment of conjunctivitis.
3. Blanket antibiotic therapy (intermittent treatment). In endemic

areas to minimise the intensity and severity of disease.

1 percent tetracycline eye ointment twice daily for 5 days in

a month for 6 months.

ADULT INCLUSION CONJUNCTIVITIS
It is a type of acute follicular conjunctivitis associated
with mucopurulent discharge. It usually affects the
sexually active young adults.
Inclusion conjunctivitis is caused by serotypes D to K of

Chlamydia trachomatis.
The primary source of infection is urethritis in males and

cervicitis in females.

The transmission of infection may occur to eyes
either through contaminated fingers or more
commonly through contaminated water of swimming
pools (hence the name swimming pool conjunctivitis).

Clinical features
Incubation period of the disease is 4-12 days.
Symptoms
Ocular discomfort, foreign body sensation,
Mild photophobia, and
Mucopurulent discharge from the eyes.


Signs of inclusion conjunctivitis are:
Conjunctival hyperaemia, more marked in fornices.
Acute follicular hypertrophy predominantly of lower

palpebral conjunctiva

Superficial keratitis in upper half of cornea.
Sometimes, superior micropannus may also occur.
Pre-auricular lymphadenopathy is a usual finding

Signs of acute fol icular conjunctivitis.
Treatment
Topical therapy.
1.It consists of tetracycline (1%) eye ointment 4 times a day for 6

weeks.

2. Systemic therapy is very important, since the condition is often

associated with an asymptomatic venereal infection.

Commonly employed antibiotics are:

Tetracycline 250 mg four times a day for 3-4weeks.
Erythromycin 250 mg four times a day for 3-4weeks

CHRONIC BACERTIAL/CATARRHAL CONJUNCTIVITIS

`Chronic catarrhal conjunctivitis' also known as
`simple chronic conjunctivitis' is characterised by
mild catarrhal inflammation of the conjunctiva.
Etiology
A. Predisposing factors
1. Chronic exposure to dust, smoke, and chemical irritants.
2. Local cause of irritation such as trichiasis, concretions, foreign body and

seborrhoeic scales.

3. Eye strain due to refractive errors, phorias or convergence insufficiency.
4. Abuse of alcohol, insomnia and metabolic disorders.
B. Causative organisms
Staphylococcus aureus is the commonest cause of chronic bacterial

conjunctivitis.

Gram negative rods such as Proteus mirabilis, Klebsiella pneumoniae,

Escherichia coli and Moraxella lacunata are other rare causes.

C. Source and mode of infection. Chronic conjunctivitis

may occur:

1. As continuation of acute mucopurulent conjunctivitis when

untreated or partially treated.

2. As chronic infection from associated chronic dacryocystitis,

chronic rhinitis or chronic upper respiratory catarrh.

3. As a mild exogenous infection which results from
direct contact, air-borne or material transfer of infection.
Clinical picture
Symptoms of simple chronic conjunctivitis include:
Burning and grittiness in the eyes, especially in the evening.
Mild chronic redness in the eyes.
Feeling of heat and dryness on the lid margins.
Difficulty in keeping the eyes open.
Mild mucoid discharge especially in the canthi.
Off and on lacrimation.
Feeling of sleepiness and tiredness in the eyes.

Signs
Ocular examination may reveal:
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 betreated 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

Characterised by mild grade inflammation confined to the

conjunctiva and lid margins near the angles associated with

maceration of the surrounding skin.

Etiology
1. Predisposing factors are same as for 'simple chronic conjunctivitis'.
2. Causative organisms. Moraxella axenfeld is the commonest

causative organism.

3.Source of infection is usually nasal cavity.
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.

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.


Phlyctenular conjunctivitis

Viral conjunctivitis
A. Acute serous conjunctivitis
B. Acute hemorrhagic conjunctivitis
C. Acute follicular conjunctivitis.