Allergic conjunctivitis is inflammation of the conjunctiva (the membrane covering the white part of the eye) due to allergy.Although allergens differ among patients, the most common cause is hay fever. Symptoms consist of redness (mainly due to vasodilation of the peripheral small blood vessels), edema (swelling) of the conjunctiva, itching, and increased lacrimation (production of tears). If this is combined with rhinitis, the condition is termed allergic rhinoconjunctivitis. The symptoms are due to release of histamine and other active substances by mast cells, which stimulate dilation of blood vessels, irritate nerve endings, and increase secretion of tears. Treatment of allergic conjunctivitis is by avoiding the allergen (e.g., avoiding grass in bloom during "hay fever season") and treatment with antihistamines, either topical (in the form of eye drops), or systemic (in the form of tablets). Antihistamines, medications that stabilize mast cells, and nonsteroidal anti-inflammatory drugs (NSAIDs) are generally safe and usually effective.

1. University of Gondar
Department of Optometry
Allergic conjunctivitis

2. ALLERGIC CONJUNCTIVITIS
• It is the inflammation of conjunctiva due to
allergic or hypersensitivity reactions which
may be immediate(humoral) or delayed
(cellular).

3. TYPES
1. Simple allergic conjunctivitis
 Hay fever conjunctivitis
 Seasonal allergic conjunctivitis (SAC)
 Perennial allergic conjunctivitis (PAC)
2. Vernal keratoconjunctivitis (VKC)
3. Atopic keratoconjunctivitis (AKC)
4. Giant papillary conjunctivitis (GPC)
5. Phlyctenular keratoconjunctivitis (PKC)
6. Contact dermoconjunctivitis (CDC)

4. SIMPLE ALLERGIC CONJUNCTIVITIS
• It is a mild, non-specific allergic conjunctivitis
characterized by itching, hyperaemia and mild
papillary response.
• It is an acute or subacute conjunctivalreaction
to allergens.

5. Etiology
 Grass pollens
 Animal dandruff
House dust and,
Mite

6. PATHOPHYSIOLOGY
• Pathological features of simple allergic
conjunctivitis comprise vascular, cellular and
conjunctival responses.
1.Vascular response is characterised by
sudden and extreme vasodilation and
increased permeability of vessels leading to
exudation.

7. …PATHOPHYSIOLOGY
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.

8. CLINICAL FEATURES
Symptoms
• intense itching
• Burning sensation
• waterydischarge
• mild photophobia.
Signs
• Hyperaemia
• chemosis
• mild papillary reaction
• edema of lids

9. DIAGNOSIS
• Diagnosisis made from:
a. typical symptoms and signs
b. normal conjunctival flora and
c. presence of abundant eosinophils in the
discharge

10. VERNAL KERATOCONJUNCTIVITIS (VKC) OR
SPRING CATARRH
• It is a recurrent, bilateral, interstitial, self-
limiting, allergic inflammation of the
conjunctiva having a periodic seasonal
incidence.
• It is considered as a hypersensitivity reaction
to some exogenous allergens.

11. ETHIOLOGY
• grass pollens

12. PREDISPOSING FACTORS
1.Age
• 4-20 years
2.sex
• more common in boys than girls.
3.Season
• More common in summer.
• Recently, it is being labelled as 'Warm weather
conjunctivitis'
3. Climate.
• More prevalent in tropics, less in temperate zones and
almost non-existent in coldclimate.

13. PATHOPHYSIOLOGY
1.Conjunctival epithelium hyperplasia
2.Marked cellular infiltration in the Adenoid
layer
3. Proliferation of fibrous layer which later on
undergoes hyaline changes.
4. proliferation,increased permeability and
vasodilation of Conjunctival vessels.

14. Symptoms
• Marked burning and itching sensation
- Itching is more marked with palpebral form of
disease
• Mild photophobia
• Lacrimation,
• Stringy (ropy) discharge and heaviness of lids

15. SIGNS
Described in following three clinical forms:
1.Palpebral VKC - upper tarsus
• papillae - hard, flat topped arranged in a
'cobble-stone' or 'pavement stone', fashion
- In severe cases, 'giant papillae'.
• white ropy discharge

16. …SIGNS
2.Bulbar VKC
• Dusky red triangular congestion of bulbar
conjunctiva
• Gelatinous thickened accumulation of tissue
around the limbus
• Presence of discrete whitish raised dots along
the limbus (Tranta's spots)
3.Mixed VKC
It shows combined features of both palpebral and
bulbar forms

17. KERATOPATHY
It is due to corneal involvement in VKC. The
following are some of corneal lesions due to
VKC.
• Superior punctate epithelial keratitis
• Ulcerative vernal keratitis (shield ulceration)
• Vernal corneal plaques
• Subepithelial scarring
• Pseudogerontoxon

18. Atopic keratoconjunctivitis (AKC)
• Adult equivalent of vernal keratoconjunctivitis
and is often associated with atopic dermatitis.
Most of the patients are young atopic adults,
with male predominance.

19. Pathophysiology
• The underlying mechanism is thought to be a
combined type I and type IV hypersensitivity
response.
• AKC has a protracted course with
exacerbations and remissions. AKC tends to be
perennial and is often worse in the winter.
• Like vernal keratoconjunctivitis it tends to
become inactive when the patient reaches the
fifth decade.

20. Symptoms
• Itching, soreness, dry sensation.
• Mucoid discharge.
• Photophobia
• blurred vision

21. Signs
• Lid margins are chronically inflamed with
rounded posterior borders.
• Tarsal conjunctiva has a milky appearance.
There are very fine papillae, hyperaemia and
scarring with shrinkage.
• Cornea may show punctate epithelial
keratitis, often more severe in lower half.
There may also occur corneal vascularization,
thinning and plaques.

22. Diagnosis
• Diagnosis is clinical but can be aided by raised
serum and tear IgE levels.
• Symptoms are similar to those of VKC, but are
frequently more severe and unremitting.
• Discharge is generally more watery than the
stringy mucoid discharge in VKC.

23. GIANT PAPILLARY CONJUNCTIVITIS (GPC)
• It is the inflammation of conjunctiva with
formation of very large sized papillae.

24. Etiology
• It is a localised allergic response to a physically
rough or deposited surface (contact lens,
prosthesis, left out nylon sutures). Probably it
is a sensitivity reaction to components of the
plastic leached out by the action of tears.

25. Pathophysiology
• GPC can occur secondary to a variety of
mechanical stimuli of the tarsal conjunctiva. It
is most frequently encountered with contact
lens (CL) wear, termed as when it is termed
contact lens-associated papillary conjunctivitis
(CLPC).

26. Signs and Symptoms
• Itching, stringy discharge and reduced
wearing time of contact lens.
• Signs
 Papillary hypertrophy (1 mm in diameter) of
the upper tarsal conjunctiva, similar to that
seen in palpebral form of VKC with
hyperaemia are the main sign.
Substantial CL protein deposits may be
present.

27. 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.

28. Etiology
• It is believed to be a delayed hypersensitivity
(Type IV-cell mediated) response to
endogenous microbial proteins.
I. Causative allergens
 Staphylococcus proteins
 Other allergens may be proteins of Moraxella
Axenfeld bacillius and certain parasites
(worm infestation).

29. Pathophysiology
1. Stage of nodule formation : exudation and
infiltration of leucocytes into the deeper layers of
conjunctiva leading to a nodule formation.
2. Stage of ulceration. Later on necrosis occurs at
the apex of the nodule and an ulcer is formed.
3. Stage of granulation. Eventually floor of the ulcer
becomes covered by granulation tissue.
4. Stage of healing. Healing occurs usually with
minimal scarring.

30. Symptoms
• mild discomfort in the eye
• irritation and reflex watering.
• May be associated mucopurulent
conjunctivitis due to secondary bacterial
infection.

31. Signs.
• The phlyctenular conjunctivitis can present in three
forms.
1. Simple phylctenular conjunctivitis. It is characterised by
the presence of a typical pinkish white nodule
surrounded by hyperaemia on the bulbar conjunctiva,
usually near the limbus.
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: characterised by the
presence of multiple phlyctens which may be arranged
in the form of a ring around the limbus and may even
form a ring ulcer.

32. Differential diagnosis
• Phlyctenular conjunctivitis needs to be
differentiated from episcleritis, scleritis.
• Presence of one or more whitish raised
nodules on the bulbar conjunctiva near the
limbus, with hyperaemia usually of the
surrounding conjunctiva, are the diagnostic
features of the phlyctenular conjunctivitis.

33. CONTACT DERMOCONJUNCTIVITIS
• It is an allergic disorder, involving conjunctiva
and skin of lids along with surrounding area of
face.

34. Etiology
• It is in fact a delayed hypersensitivity (type IV)
response to prolonged contact with chemicals
and drugs. A few common topical ophthalmic
medications known to produce contact
dermoconjunctivitis are atropine, penicillin,
neomycin, soframycin and gentamycin.

35. Clinical features
• Cutaneous involvement is in the form of
weeping eczematous reaction, involving all
areas with which medication comes in
contact.
• 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.

36. Diagnosis
• 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.

37. Managements startegies of allergic
conjunctivitis
• Avoiding allergen that trigger may be the best
solution.
• Definitive( pharmachologic) management
• Supportive management

38. 1.Ocular Decongestants
Mechanism of action
• This drugs are adrenergic agonist mainly alpha 1
receptor
• Local vasoconstrictor, temporarily reduces redness
and swallowen blood vessel
Example : Phenylephrine (action-selective alpha one
agonist).

39. Mechanism of action
• Blocks H1 receptors which control
.Itching
.Capillary dilation
.Increase in capillary permeability
• Thus providing symptomatic relief from
histamine activity.
Antihistamins

40. Some antihistamine drugs
• Pheniramine, antazoline combined with
naphazoline
• Levocabastine HCl ophthalmic suspension
0.5% (Livostin)
• Emedastine difumarate 0.05% (Emadine)

41. Mast cell stabilizer
Mechanism of action
-Mast cell stabilizers work by inhibiting mast cell
degranulation thereby reducing the release of inflammatory
substances.
- However, these agents do not eliminate inflammatory
mediators that have released prior to drug instillation.
Effective for VKC,AKC,GPC
Examples
•Cromolyn Sodium (Sodium cromoglycate) 4%
• Lodoxaminde 0.1%
• Pemirolast potassium 0.1% (Alamast)
• Nedocromil sodium 2% (Alocril)

42. Corticosteroids
 Mechanism of action
-By inhibiting phospholipase A2 ,block the release of
arachidonic acid and its subsequent conversion to
eicosanoids.
-Inhibition of degranulation of mast cells, basophils and
neutrophils.
Examples
• Dexamethasone/0.1%/
• Fluorometholone 0.1%
• prednisolone acetate (0.125% and 1.0%)
N.B corticosteroids should be tapered, as our body has
corticoid hormones.

43. NSAIDs
Mechanism of action
• NSAIDs inhibit prostaglandin production from
arachidonic acid by blocking cyclooxygenase. which
results in vasoconstriction, decrease in vascular permeability.
• It penetrates the cornea & reaches concentrations
that reduces prostaglandin E levels in the aqueous
humor.
example : Ketorolac tromethamine 0.5%
Used for

44. some supportive managements
• Cold compress
• Artificial tear