Vous êtes sur la page 1sur 13

CONJUNCTIVITIS

Conjunctivitis
Inflammation of the conjunctiva (conjunctivitis) is classically defined as conjunctival
hyperaemia associated with a discharge which may be watery, mucoid, mucopurulent or
purulent.
Etiology
Causes of conjunctivitis maybe fallin to two broad categories:
Infectious:
bacterial
viral
parasitic
mycotic !
Noninfectious(seeFig.4.4)
from a persistent irritation (such as lack of tear fluid or uncorrected refractive
error;seeFig.4.4)
allergic
toxic(duetoirritants such as smoke, dust, etc.)
asaresultofanotherdisorder(suchasStevensJohnsonsyndrome).
Clinical features of conjunctival inflammation
1) Symptoms
Non-specific symptoms include lacrimation, grittiness, stinging and burning. Itching is
the hallmark of allergic disease, although it may also occur to a lesser extent in
blepharitis and dry eye. Significant pain, photophobia or a marked foreign body
sensation suggest corneal involvement.
2) Discharge
Watery discharge is composed of a serous exudate and tears, and occurs in acute
viral or acute allergic conjunctivitis.
Mucoid discharge is typical of chronic allergic conjunctivitis and dry eye.
Mucopurulent discharge typically occurs in chlamydial or acute bacterial
infection.
Moderately purulent discharge occurs in acute bacterial conjunctivitis.
Severe purulent discharge is suggestive of gonococcal infection.

3) Conjunctival reaction
o Hyperaemia that is diffuse, beefy-red and more intense away from the limbus is
usual in bacterial infection. This conjunctival injection should be distinguished
from the ciliary injection of iridocyclitis.
o Haemorrhages may occur in viral conjunctivitis, when they are often multiple,
small and discrete, and severe bacterial conjunctivitis, when they are larger and
diffuse.

o Chemosis (conjunctival oedema) is seen as a translucent swelling, which when


severe may protrude through the eyelids. Acute chemosis usually indicates a
hypersensitivity response (e.g. pollen), but can also occur in severe infective
conjunctivitis. Subacute or chronic chemosis has numerous causes:
o Local, e.g. thyroid eye disease, chronic allergic conjunctivitis, ocular or
eyelid surgery, trauma.
o Increased systemic vascular permeability, e.g. allergic conditions,
infections including meningitis, vasculitis.
o Increased venous pressure, e.g. superior vena cava syndrome, right-sided
heart failure.
o Decreased plasma oncotic pressure, e.g. nephrotic syndrome.

o Membranes
o Pseudomembranes consist of coagulated exudate adherent to the inflamed
conjunctival epithelium. They can be peeled away leaving the underlying
epithelium intact.
o True membranes involve the superficial layers of the conjunctival
epithelium so that attempted removal leads to tearing. The distinction
between a true membrane and a pseudomembrane is rarely clinically
helpful and both can leave scarring following resolution.

o Causes include severe adenoviral conjunctivitis, gonococcal and some


other bacterial conjunctivitides (Streptococcus spp., Corynebacterium
diphtheriae), ligneous conjunctivitis and StevensJohnson syndrome

o Infiltration represents cellular recruitment to the site of chronic inflammation


and typically accompanies a papillary response. It is recognized by loss of detail
of the normal tarsal conjunctival vessels, especially on the upper lid

o Subconjunctival cicatrization (scarring) may occur in trachoma and other


severe conjunctivitides.Severe scarring is associated with loss of goblet cells and
accessory lacrimal glands, and can lead to cicatricial entropion.
o Follicles Multiple, discrete, slightly elevated lesions resembling translucent
grains of rice, most prominent in the fornices (Fig. 5.3A). Blood vessels run
around or across rather than within the lesions.

o Papillae can develop only in the palpebral conjunctiva and in the limbal bulbar
conjunctiva where it is attached to the deeper fibrous layer. Signs. In contrast to
follicles, a vascular core is present. Micropapillae form a mosaic-like pattern of
elevated red dots as a result of the central vascular channel.

4) Lymphadenopathy
The most common cause of lymphadenopathy associated with conjunctivitis is viral
infection. It may also occur in chlamydial and severe bacterial conjunctivitis
(especially gonococcal), and Parinaud oculoglandular syndrome. The preauricular site
is typically affected.

Bacterial Conjunctivitis
Acute bacterial conjunctivitis Acute bacterial conjunctivitis is a common and usually
selflimiting condition caused by direct contact with infected secretions. The most common
isolates are Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae and
Moraxella catarrhalis. A minority of cases, usually severe, are caused by the sexually
transmitted organism Neisseria gonorrhoeae, which can readily invade the intact corneal
epithelium. Meningococcal (Neisseria meningitidis) conjunctivitis is rare, and usually affects
children.
Diagnosis
Symptoms
o Acute onset of redness, grittiness, burning and discharge.
o Involvement is usually bilateral although one eye may become affected 12 days before
the other.
o On waking, the eyelids are frequently stuck together and may be difficult to open.
o Systemic symptoms may occur in patients with severe conjunctivitis associated with
gonococcus, meningococcus, Chlamydia and H. influenzae. In children, the possibility
of progression to systemic involvement should always be borne in mind
Signs are variable and depend on the severity of infection.
o Eyelid oedema and erythema (Fig. A) may occur in severe infection, particularly
gonococcal.
o Conjunctival injection as previously described (Fig. B).
o The discharge can initially be watery, mimicking viral conjunctivitis, but rapidly
becomes mucopurulent (Fig. C).
o Hyperacute purulent discharge (Fig. D) may signify gonococcal or meningococcal
conjunctivitis.
o Superficial corneal punctate epithelial erosions are common.
o Peripheral corneal ulceration may occur in gonococcal and meningococcal infection,
and may rapidly progress to perforation.
o Lymphadenopathy is usually absent except in severe gonococcal and meningococcal
infection.

Treatment
About 60% resolve within 5 days without treatment.
Topical antibiotics, usually four times daily for up to a week but sometimes more
intensively, are frequently administered to speed recovery and prevent re-infection
and transmission. There is no evidence that any particular antibiotic is more effective.
Ointments and gels provide a higher concentration for longer periods than drops but
daytime use is limited because of blurred vision. The following antibiotics are
available: Chloramphenicol, aminoglycosides (gentamicin, neomycin, tobramycin),
quinolones (ciprofloxacin, ofloxacin, levofloxacin, lomefloxacin, gatifloxacin,
moxifloxacin, besifloxacin), macrolides (erythromycin, azithromycin) polymyxin B,
fusidic acid and bacitracin.
Systemic antibiotics are required in the following circumstances: Gonococcal
infection is usually treated with a thirdgeneration cephalosporin such as ceftriaxone;
quinolones and some macrolides are alternatives; H. influenzae infection,
particularly in children, is treated with oral amoxicillin with clavulanic acid; there is a
25% risk of developing otitis and other systemic problems. Meningococcal
conjunctivitis, also particularly in children, in whom early systemic prophylaxis may
be life-saving as up to 30% develop invasive systemic disease.
Topical steroids may reduce scarring in membranous and pseudomembranous
conjunctivitis, although evidence for their use is unclear.
Irrigation to remove excessive discharge may be useful in hyperpurulent cases.
Contact lens wear should be discontinued until at least 48 hours after complete
resolution of symptoms.
Risk of transmission should be reduced by hand-washing and the avoidance of
towel sharing.
Review is unnecessary for most mild/moderate adult cases, although patients should
be cautioned to seek further advice in the event of deterioration.

VIRAL CONJUNCTIVITIS
Viral conjunctivitis is a common external ocular infection, adenovirus (a non-enveloped
double-stranded DNA virus) being the most frequent (90%) causative agent. It may be
sporadic, or occur in epidemics in environments such as workplaces (including hospital),
schools, and swimming pools. The spread of this highly contagious infection is facilitated by
the ability of viral particles to survive on dry surfaces for weeks, and by the fact that viral
shedding may occur for many days before clinical features are apparent. Transmission is
generally by contact with respiratory or ocular secretions, including via fomites such as
contaminated towels
Presentation
The spectrum of viral conjunctivitis varies from mild subclinical disease to severe
inflammation with significant morbidity. There will often be a history of a close contact with
acute conjunctivitis.
o Non-specific acute follicular conjunctivitis is the most common clinical form of
viral conjunctivitis, and is typically due to adenoviral infection by a range of
serological variants. Unilateral watering, redness, irritation and/or itching, and mild
photophobia occur, the contralateral eye generally being affected 12 days later, often
less severely.
o Pharyngoconjunctival fever (PCF) is caused mainly by adenovirus serovars 3, 4 and
7. It is spread by droplets within families with upper respiratory tract infection.
o Epidemic keratoconjunctivitis (EKC) is caused mainly by adenovirus serovars 8, 19
and 37, and is the most severe ocular adenoviral infection.
o Acute haemorrhagic conjunctivitis usually occurs in tropical areas. It is typically
caused by enterovirus and coxsackievirus, though other microorganisms may present
similarly.
o Chronic/relapsing adenoviral conjunctivitis giving a chronic non-specific
follicular/papillary clinical picture can persist over years, but is rare and eventually
self-limiting.
o Herpes simplex virus (HSV) can cause a follicular conjunctivitis, particularly in
primary infection; this is usually unilateral and there are often associated skin
vesicles.
o Systemic viral infections such as those common in childhood, e.g. varicella, measles
and mumps, can feature an associated follicular conjunctivitis; varicella-zoster virus

Signs
o Eyelid oedema ranges from negligible to severe.
o Lymphadenopathy is common: tender pre-auricular.
o Conjunctival hyperaemia and folliclesare typically prominent; papillae may
also be seen, particularly in the superior tarsal conjunctiva.
o Severe inflammation may be associated with conjunctival haemorrhages
(usually petechial in adenoviral infection see Fig. B), chemosis, membranes
(rare) and pseudomembranes, sometimes with conjunctival scarring after
resolution.

o Keratitis (adenoviral).
o Anterior uveitis is sometimes present, but is mild.
o Molluscum contagiosum.
- A pale, waxy, umbilicated nodule on the lid margin (Fig. A) associated with
follicular conjunctivitis (Fig. B) and mild watery and mucoid discharge.
- Bulbar nodules and confluent cutaneous lesions may occur in
immunocompromised patients.
Treatment
Spontaneous resolution of adenoviral infection usually occurs within 23 weeks, so
specific treatment is typically unnecessary.
Reduction of transmission risk by meticulous hand hygiene, avoiding eye rubbing
and towel sharing. There should be scrupulous disinfection of instruments and clinical
surfaces after examination of an infected patient (e.g. sodium hypochlorite, povidone-
iodine).
Molluscum contagiosum. Although lesions are self-limiting in immunocompetent
patients.
Topical steroids such as prednisolone 0.5% four times daily may be required for
severe membranous or pseudomembranous adenoviral conjunctivitis.
Other measures : Discontinuation of contact lens wear until resolution of symptoms,
artificial tears four times daily may be useful for symptomatic relief. Preservative-free
preparations may give superior comfort, and if supplied in single-dose units may
reduce transmission risk, and Cold (or warm) compresses for symptomatic relief.

ALLERGIC CONJUNCTIVITIS
Atopy is a genetically determined predisposition to hypersensitivity reactions upon exposure
to specific environmental antigens. Clinical manifestations include the various forms of
allergic conjunctivitis, as well as hay fever (seasonal allergic rhinitis), asthma and eczema.
Allergic conjunctivitis is a Type I (immediate) hypersensitivity reaction, mediated by
degranulation of mast cells in response to the action of IgE; there is evidence of an element of
Type IV hypersensitivity in at least some forms.
Acute allergic conjunctivitis
Acute allergic conjunctivitis is a common condition caused by an acute conjunctival reaction
to an environmental allergen, usually pollen. It is typically seen in younger children after
playing outside in spring or summer. Acute itching and watering are common, but the
hallmark is chemosis (Figs A and B), which is frequently dramatic and worrying to the child
and parents. Treatment is not usually required and the conjunctival swellingsettles within
hours as the acute increase in vascular permeability resolves. Cool compresses can be used
and a single drop of adrenaline 0.1% may reduce extreme chemosis.

Seasonal and perennial allergic conjunctivitis


These common subacute conditions are distinguished from each other by the timing of
exacerbations, thought to relate principally to differing stimulating allergens in each.
Seasonal allergic conjunctivitis (hay fever eyes), worse during the spring and
summer, is the more common. The most frequent allergens are tree and grass pollens,
although the specific allergen varies with geographic location.
Perennial allergic conjunctivitis causes symptoms throughout the year, generally
worse in the autumn when exposure to house dust mites, animal dander and fungal
address allergent is greates.
Diagnosis
Symptoms. Transient acute or subacute attacks of redness, watering and itching, associated
with sneezing and nasal discharge.
Signs. Conjunctival hyperaemia with a relatively mild papillary reaction, variable chemosis
and lid oedema.
Investigations are generally not performed although conjunctival scraping in more active
cases may demonstrate the presence of eosinophils. Skin testing for particular allergens is
rarely required.

Treatment
Artificial tears for mild symptoms.
Mast cell stabilizers (e.g. sodium cromoglicate, nedocromil sodium, lodoxamide)
must be used for a few days before exerting maximal effect, but are suitable (except
lodoxamide) for long-term use if required.
Antihistamines (e.g. emedastine, epinastine, levocabastine, bepotastine) can be used
for symptomatic exacerbations and are as effective as mast cell stabilizers.
Dual action antihistamine and mast cell stabilizers (e.g. azelastine, ketotifen,
olopatadine) act rapidly and are often very effective for exacerbations.
Combined preparation of an antihistamine and a vasoconstrictor (e.g. antazoline
with xylometazoline).
Non-steroidal anti-inflammatory preparations (e.g. diclofenac) can provide
symptomatic relief but are rarely used.
Topical steroids are effective but rarely necessary.
Oral antihistamines may be indicated for severe symptoms. Some, such as
diphenhydramine, cause significant drowsiness and may be useful in aiding sleep;
others, such as loratadine, have a far less marked sedative action.

CHLAMYDIAL CONJUNCTIVITIS
Chlamydia lie midway between bacteria and viruses, sharing some of the properties of
both. Like viruses, they are obligate intracellular and filterable, whereas like bacteria they
contain both DNA and RNA, divide by binary fission and are sensitive to antibiotics.
The chlamydia combinedly form the PLT group (Psittacosis, Lymphogranuloma
venereum and Trachomatis group).

Life cycle of the chlamydia. The infective particle invades the cytoplasm of epithelial cells,
where it swells up and forms the 'initial body'. The initial bodies 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. Jones' has classified chlamydial


infections of the eye into following three classes :
Class 1 : Blinding trachoma. Blinding trachoma refers to hyperendemic trachoma
caused by serotypes A, B, Ba and C of Chlamydia trachomatis associated with secondary
bacterial infection. It is transmitted from eye to eye by transfer of ocular discharge through
various modes.
Class 2 : Non-blinding trachoma. It is also caused by 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 socioeconomic conditions. It is a
mild form of disease with limited transmission owing to improved hygiene.
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
Trachoma (previously known as Egyptian ophthalmia) is a chronic keratoconjunctivitis,
primarily affecting the superficial epithelium of conjunctiva and cornea simultaneously. It is
characterised by a mixed follicular and papillary response of conjunctival tissue. It is still one
of the leading causes of preventable blindness in the world. The word 'trachoma' comes from
the Greek word for 'rough' which describes the surface appearance of the conjunctiva in
chronic trachoma.

Etiology
A. Causative organism. Trachoma is caused by a Bedsonian organism, the Chlamydia
trachomatis belonging to the Psittacosis-lymphogranulomatrachoma (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
microimmunofluorescence techniques. Serotypes A, B, Ba and C are associated with
hyperendemic (blinding) trachoma, while serotypes D-K are associated with
paratrachoma (oculogenital chlamydial disease).

B. Predisposing factors. These include age, sex, race, climate, socioeconomic status and
environmental factors.
1. Age. The infection is usually contracted during infancy and early childhood.
Otherwise, there isno age bar.
2. Sex. As far as sex is concerned, there is general agreement that preponderance
exists in the females both in number and in severity of disease.
3. Race. No race is immune to trachoma, but the disease is very common in Jews and
comparatively less common among Negroes.
4. Climate. Trachoma is more common in areas with dry and dusty weather.
5. Socioeconomic status. The disease is more common in poor classes owing to
unhygienic living conditions, overcrowding, unsanitary conditions, abundant fly
population, paucity of water, lack of materials like separate towels and
handkerchiefs, and lack of education and understanding about spread of
contagious diseases.
6. Environmental factors like exposure to dust, smoke, irritants, sunlight etc.
increase the risk of contracting disease. Therefore, outdoor workers are more
affected in comparison to office workers.

C. Source of infection. In trachoma endemic zones the main source of infection is the
conjunctival discharge of the affected person. Therefore, superimposed bacterial
infections help in transmission of the disease by increasing the conjunctival
secretions.

D. Modes of infection. Infection may spread from eye to eye by any of the following
modes:

1. Direct spread of infection may occur through contact by air-borne or water-borne


modes.
2. Vector transmission of trachoma is common through flies.
3. Material transfer plays an important role in the spread of trachoma. Material
transfer can occur through contaminated fingers of doctors, nurses and
contaminated tonometers. Other sources of material transfer of infection are use of
common towel, handkerchief, bedding and surma-rods.

Prevalence
Trachoma is a worldwide disease but it is highly prevalent in North Africa, Middle East and
certain regions of Sourth-East Asia. It is believed to affect some 500 million people in the
world. There are about 150 million cases with active trachoma and about 30 million having
trichiasis, needing lid surgery. Trachoma is responsible for 15-20 percent of the world's
blindness, being second only to cataract.

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
1. Congestion of upper tarsal and forniceal conjunctiva.
2. Conjunctival follicles. Follicles look like boiled sagograins and are 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).
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.
Complications
The only complication of trachoma is corneal ulcer which may occur due to rubbing by
concretions, or trichiasis with superimposed bacterial infection.

Management
Management of trachoma should involve curative as well as control measures.
A. Treatment of active trachoma
The following topical and systemic therapy regimes have been recommended:
1. Topical therapy regimes. It is best for individual cases. It 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. 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.
3. Combined topical and systemic therapy regime.
It is preferred when the ocular infection is severe (TI) or when there is associated
genital infection It includes: (i) 1 per cent tetracycline or erythromycin eye ointment 4
times a day 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 should be removed with a hypodermic needle.
2. Trichiasis may be treated by epilation, electrolysis or cryolysis
3. Entropion should be corrected surgically
4. Xerosis should be treated by artificial tears.

C. Prophylaxis
Following prophylactic measures may be helpful against reinfection of trachoma.
1. Hygienic measures. These help a great deal in decreasing the transmission of disease, as
trachoma is closely associated with personal hygiene and environmental sanitation.
Therefore, health education on trachoma should be given to public. 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 ofconjunctivitis should be treated as early as


possible to reduce transmission of disease.

3. Blanket antibiotic therapy (intermittent treatment). WHO has recommended this regime to
be carried out in endemic areas to minimise the intensity and severity of disease. The regime
is to apply 1 percent tetracycline eye ointment twicedaily for 5 days in a month for 6 months.
Referensi : Bowling, Brad. 2016. Kanskis Clinical Ophthalmology A SYSTEMATIC
APPROACH EIGHTH EDITION. Printed in China : ELSEVIER limited.
Khurana, A K. 2007. Comprehensive OPHTHALMOLOGY fouth eddition. New Delhi : NEW
AGE INTERNATIONAL (P) LIMITED, PUBLISHER.
Gerhard K. Lang, M. D. 2000. Opthalmology. New York : Thieme Stuttgart