1. Hira Nath Dahal
B. Optometry
Maharajgunj Medical Campus
Institute of Medicine

2. Introduction
 Allergy means altered reaction
 a hypersensitivity to a substance that causes
the body to react to any contact with that
substance
 Is a term synonymously with hypersensitivity
Ocular allergy are a group of external ocular
conditions resulting from one or more types of
hypersensitivity reactions to allergens

3. contd….
 Approx 20% of the general population have
some form of allergic disorder but about a
third of these have ophthalmic symptoms
 Most commonly affects the conjunctiva but
other mucous membranes may also be
affected as may the cornea alone or in
association with lid involvement

4. Allergy
 Four types of allergic responses
 Type I- Immediate/anaphylactic reaction
 Type II- Cytotoxic reaction
 Type III- Immune complex reaction
 Type IV- cell mediated immunity

5. Type I hypersensitivity
 Ig-E mediated hypersensitivity
 The sequence of events involved in type I
hypersensitivity reaction can be divided into
three phases:
 Sensitization phase
 Activation phase(early allergic
response)
 Late allergic response

6. Sensitization
 Conjunctiva is normally exposed to pictogram
quantities of environmental allergens s/a
pollens, dust mites, fecal particles, animal
dander and other proteins
 When deposited on the mucosa these
antigens are processed by langerhans cells
and other APC in the mucosal epithelium

7.  Antigen is presented to T-lymphocyte where
the specific T-cell receptors recognize the
antigenic peptide
 T-cell produce cluster of cytokines
 The cytokines (IL3, IL4, IL5, IL6,etc) stimulate
B-cell for Ig-E production
 Mast cells are particularly abundant in the
conjunctival stroma especially at the limbus
 Mast cells bears high affinity for Ig-E are the
most important cells in Ig-E mediated
responses

9. Early phase
 Allergic reactions occur when pre-formed IgE
antibodies bound to IgE receptors on mast
cells encounter the antigen for which they
have specificity.
 Cross linkage of adjacent IgE antibodies by
antigen activates the mast cell and it
degranulates

10.  Histamines:
∞ Vasodilation, smooth muscle contraction
 Itching , redness
 Heparin
∞ Prevent blood coagulation
∞ Help to package and store other mediators in
the granules
 Tryptase
∞ Potentiates histamines, activates eosinophils
and mast cells

11.  Prostaglandin and leukotrienes
∞ Capillary leakage, smooth muscle
contraction, increase granulocyte action and
platelets aggregation
 ECF-A: attracts neutrophils
 Platelets activating factor(PAF)
∞ Platelets aggregation, neutrophil chemotaxis

12.  Eosinophils are activated by interaction of
mast cells with other inflammatory cells such
as platelet activating factor
 Activated eosinophils release very basic highly
charged polypeptide including:
 Major basic protein (MBP)
 Eosinophil cationic protein (ECP)
 Eosinophil derived neurotoxin(EPX)
 Eosinophil peroxidase (EPO)

13.  These proteins may bind to basement
membrane proteoglycans and hyaluran to
cause cellular aggregation and epithelial
desquamation
 ECP and EPX are epithelial toxic and are
involved in corneal damage that may occur in
severe chronic allergy
 ECP and EPX tear level are correlated with
clinical signs and symptoms of allergic disease
and may be considered as local markers of
eosinophils activation

15. Late phase
 Mast cell activation results in expression of
cytokine genes.
 Cytokines released in the local area of
inflammation activate inflammatory cells like
neutrophils recruited by histamine and
leukotrienes.
 Activated inflammatory cells perpetuate the
inflammatory response

17. Mediaters of allergicresponse
Mediator Activity Symptoms/Sig
ns
Histamine Stimulate nerve endings
Dilate blood vessels
Itching
Redness
Edema
Platelet activating factor Dilates blood vessels
Eosinophil recruitment
Redness, edema
Leukotrienes/Prostaglan
dins
Dilates blood vessels
Stimulate mucus
production
Redness
Stringy mucus
Proteases May degrade small
vessel basement
membrane permeability
Swelling
Eosinophil chemotactic
factor
Recruits eosinophils Prolong immune
response

18.  Type-I hypersensitivity mechanisms account
for the anaphylactic reactions to penicillin
and insect bites and for allergic reactions of
hay fever and asthma
 In addition to other hypersensitivity
mechanisms, Type-I mechanisms play a role in
more complex disorders such as vernal
keratoconjunctivitis (VKC) and giant
papillary conjunctivitis (GPC)

19. Seasonal and Perennial Allergic
Conjunctivitis
 Itching is the hallmark symptom of ocular
allergies.
 In addition to itching, SAC and PAC can also
present with bilateral
redness, burning, tearing, photophobia, and
occasionally stringy mucous discharge.

20.  Swelling of the eyelids is usually present, and the eyes
will have a glassy look due to conjunctival swelling
figure shows the mild
hyperemia, chemosis, and glassy
appearance of the eye typically seen in

21.  Patients with SAC often present with mild to
moderate conjunctival injection and
chemosis
 Chemosis usually more prominent in the
nasal conjunctiva because the conjunctiva is
more loosely attached in this area.
 Swelling of the eyelids may cause a
narrowing of the intrapalpebral fissure, and
papillae may be present on the palpebral
conjunctiva.

22.  The ocular symptoms of SAC and PAC are
reoccurring and are exacerbated during pollen
season or in the presence of specific antigens.
 Patients with SAC usually have a family or
personal history of food or environmental
allergies including PAC, asthma, or eczema.
 Although the eye may be the only organ
involved, nasal symptoms and sneezing are
frequently reported.

23. Vernal keratoconjunctivitis
 Because of the potential for vision loss, it is
critical that the acute forms of ocular allergies
such as SAC and PAC are correctly
differentiated from sight-threatening ocular
allergies such at VKC and AKC
 The most common sensitizing agent producing
VKC is rye grass with other common causes
being pollen, dust mites, and animal dander.
Non-specific factors such as sun, dust, and
wind exposure can also trigger the onset of
VKC

24.  Bilateral intense itching is characteristic of
VKC, but
tearing, photophobia, blepharospasm, blurr
ed vision, stringy discharge, and difficulty
opening the eyes in the morning are also
commonly reported.
 Patients may also report pain if the cornea
becomes involved

25.  VKC patients typically have seasonal
exacerbations, but at least 60% of them have
recurrences year-round.
 For those with seasonal exacerbations, the
most severe appearance of the disease
usually occurs in the spring. Approximately
16% of patients with seasonal exacerbations
progress to experiencing perennial VKC
symptoms

26.  Nearly 49% of patients who suffer from VKC
have a family history of atopic disease such as
asthma, rhinitis, or eczema.
 VKC is also commonly associated with a
personal allergy history, which might include
asthma, rhinitis, or atopic eczema

27.  Clinically 2 forms of VKC may be seen:
Palpebral
Limbal &
May be mixed

28. Palpebral VKC:
Diffuse papillary hypertrophy more prominent
on upper tarsus rather than lower region
Bulbar conjunctiva hyperemia/chemosis may be
seen
In severe cases, giant papillae resembles
cobbblestones in upper tarsus

29.  Limbal VKC:
May develop alone or in association with
palpebral VKC
Limbus has thickened, gelatinous appearance
with scattered opalescent mounds and
vascular injection

30.  Horner-Trantas dots, whitish dots that
represent macroaggregates of degenerated
eosinohils and epithelial cells may be
observed in the hypertrophied limbus of pts
with limbal VKC

31.  Ninety-eight percent of VKC presentations
are bilateral, but the presentation severity can
be asymmetric
 Corneal complications are common in patients
with VKC. Early signs of corneal involvement
include punctate erosions, which can coalesce
to form macroerosions that can be quite
painful. Inflammatory debris often accumulates
in the macroerosion forming an opaque
plaque, which can prevent epithelialization of
the cornea

32.  These non-healing epithelial defects, also
known as shield ulcers, are typically oval in
shape and located superiorly.
Shield ulcer in vernal
keratoconjunctivitis

33.  It is thought that corneal damage producing
shield ulcers might be due to eosinophil
granule major basic protein (MBP) substance.
 Large amounts of MBP have been found in
tears and ocular tissues of VKC patients, and
this substance can damage tissue and slow
wound repair.
 It has also been hypothesized that shield
ulcers can be caused by mechanical abrasion
of the cornea, possibly due to eye rubbing.

34.  Ulcers make the eye more susceptible to
secondary infections, especially when the VKC
is treated with topical steroids.
 Other complications of shield ulcers can
include corneal vascularization, corneal
opacification and amblyopia in children.

35. Giant papillary
conjunctivitis
 Cause of GPC is an allergic reaction to protein
deposits on contact lenses.
 Both a mechanical and an immunologic
process have been suggested as the reason for
hypersensitivity to theses deposits.
 The time of onset between a soft contact lens
fitting and the onset of GPC is usually between
10 to 20 months for patients who will
experience this problem.
 The condition is most often bilateral but can
be asymmetric; only 10% of cases are
unilateral.

36.  A coated or poorly fitting contact lens can
produce trauma to the tarsal conjunctiva,
which aids in development of GPC by allowing
allergens on the contact lens to be exposed to
the immune system.
 Immunological cells, e.g. mast cells and
eosinophils, are present and IgE is found in
the tears of patients with GPC

37.  GPC can occur with any type of contact lens
including high Dk silicone hydrogel contact
lenses.
 Lenses that have a higher water content tend
to have more deposits and lenses that are
ionically charged also tend to attract more
proteins.

38.  Symptoms of GPC include itching, foreign
body sensation, blurred vision, increased
mucus production, and contact lens
intolerance.
 Patients will also often complain about mucus
in the nasal canthus, especially upon
wakening.
 Symptoms are not as severe as for VKC, but
the appearance can be similar to advanced
cases of GPC.

39.  The signs of GPC consist of
hyperemia, thickening, and abnormally large
papillae (diameter >0.3 mm) on the superior
tarsal conjunctiva
Giant papillary
conjunctivitis

40.  Treatment of GPC involves removal of the
offending agent if possible. This includes
improved contact lens hygiene, the use of
disposable contact lenses, and/or modifying
the contact lens design.
 The type of pharmacological therapy usually
depends on the degree of the condition. Mast
cell stabilizers and topical steroids have been
shown to be effective in the treatment of
GPC, but long-term use of steroids is not
recommended due to the risk of potential side-
effects

41.  Refitting GPC patients with a different contact
lens material has been shown to allow more
than 80% of patients to wear lenses without
further GPC symptoms.
 Providing patients with a more frequent
replacement schedule can also help. This
approach has allowed 91% of patients to
continue wearing contacts symptom-free.

42.  Wearing contact lenses for three weeks or less
before replacement significantly decreases the
incidence of GPC as compared to wearing
them four weeks or longer.
 Redness, itching, and discharge will subside
quickly following GPC treatment, but the
papillae will take a longer time to subside.
 Contact lens wear should be discouraged in
severe or recurring cases of GPC

43. Atopic keratoconjunctivitis
 Atopy is state in which individuals are
predisposed to type-I hypersensitivity
reactions, there is genetic basis whereby IgE
is synthesized more readily and in greater
amounts to irrelevant antigens
 Have depressed systemic cell mediated
immunity, as a consequence they are
susceptible to herpes simplex virus keratitis
and to colonization of the eyelids with
staphylococcus aureus

44.  Symptoms of AKC include intense bilateral
itching of the eyelids and conjunctiva.
 Tearing, burning, foreign body
sensation, photophobia, and stringy ropy
discharge are also typically present.
 Although some patients experience
exacerbations in the winter and summer
months, symptoms are usually present year-
round

45.  When considering the possibility of AKC, it is
essential to obtain a thorough personal and
family history of allergic disease.
 Up to 60% of AKC patients have a family
history of allergies, and approximately 92% will
report a personal occurrence of non-ocular
allergies.
 At least 95% will have eczema, and 87% have
asthma

46.  Checking for signs of eczema is necessary
when examining patients with AKC. The
systemic manifestations of atopic dermatitis
can help to differentiate this condition from
VKC.
 Due to eczema in the periorbital area, the
eyelids tend to be thick, indurated, and red.
Ptosis is often present. Chronic
blepharitis, meibomian gland dysfunction, and
dry eye have also been associated with AKC.

47.  Papillary hypertrophy of the upper and lower
palpebral conjunctiva is a common finding in AKC
patients.
 Hyperemia and chemosis, are most prominent in
the inferior and palpebral conjunctiva. In
addition, gelatinous nodules with or without Tranta's
dots might be present

48.  Due to corneal involvement and other ocular
manifestations, AKC can have a dramatic
effect on a patient’s vision. Corneal
complications commonly occur and punctate
keratitis can be seen early in the development
of this condition.

49.  Prolonged inflammation can cause persistent
epithelial defects and plaque formation.
Secondary microbial infection, corneal
ulceration, neovascularization, and superior
pannus can also result
figure shows neovascularization produced by severe AKC

50.  Keratoconus and atopic anterior subcapsular
cataract formation are common in AKC
patients.
 It is thought that persistent eye rubbing results
in an increased risk of retinal detachment.

51. Type-II (cytotoxicity)
 Results in tissue damage d/t presence of circulating
complement fixing antibody directed against specific
antigens on the surface of particular cells or in tissue
components
 Binding of Ab to Ag leads to destruction of target cells
and tissue damage by:
Lysis of cell membrane through the activation of
complement system
Phagocytosis of the target cells by
macrophages mediated through c3b or Fc
fragments of immunoglobulin (opsonization) OR
Direct damage to the target cells through the
mechanism of ADCC

52.  Type-II hypersensitivity is the underlying
mechanism of haemolytic blood transfusion
reaction and is involved in disorders s/a
ocular cicatricial pemphigoid, pemphigus
and possibly Mooren’s ulcer

53.  The mechanism of ocular cicatricial
pemphigoid (OCP), or mucous membrane
pemphigoid (MMP), represent a cytotoxic (type
II) hypersensitivity in which cell injury results
from auto antibodies directed against a cell
surface antigen in the basement membrane
zone (BMZ)
 In pemphigus, a bullous disorder primarily of
the skin but which may also affect the
eye, antibody is directed against proteins
involved in intercellular adhesion

54. Type-III (immune complex
mediated)
 Results when Ab binds to circulating antigens
to form immune complexes which become
deposited in tissues
 If the complexes contain
immunoglobulin, activation of complement
cascade results in inflammatory response and
local tissue damage

55.  In the eye, vasculitis in party mediated by
type-III hypersensitivity
 Also involved in peripheral ulcerative
keratitis, necrotizing scleritis and Mooren’s
ulcer
If Ab is present in the excess, the immune complexes
are large and result in granulomatous inflammation
Equal amount of Ag and Ab produce moderate sized
immune complexes and the inflammatory reaction is
chronic but non-granulomatous
Excess antigen results in small immune complexes
which produce an acute vasculitis

56.  Peripheral ulcerative keratitis is associated
with other immune complex mediated disease
s/a Rheumatoid arthritis, Polyarteritis
nodosa, Wegner’s granulomatosis and
Systemic lupus erythrematosus
 Mooren’s ulcer : ulceration starts at the
corneal periphery which spreads
circumferentially & centrally exhibiting an
undetermined leading edge

57. Type IV (cell mediated)
 An antigen elicited cellular immune reactions
resulting in tissue damage
 Unlike other types doesn’t require the
participation of antibodies
 MHC class-II restricted antigen is presented to
antigen specific T lymphocytes that become
activated and release lymphokines
Triggers a complex cellular response in which other
lymphocytes, macrophages, fibroblasts and to a
lesser extent , neutrophils are recruited and
activated

58.  Tissue injury is caused by T-lymphocytes &/or
macrophages
 Caused by cell mediated cytotoxity,
phagocytosis, natural killer cell activity,
enzyme release and when antigen persists
aggregates of epitheloid cells (granulomatous
inflammation)

59.  Type-IV hypersensitivity is the basis of
granulomatous inflammation of
tuberculosis, leprosy and fungal inflammation
& sympathetic ophthalmitis
 May also be induced in viral infections and
occurs in corneal graft
rejection, phlyctenulosis, ocular
myopathies, Sjogren’s syndrome and
contact allergy of the skin and conjunctiva

60. Phlyctenular keratoconjunctivitis
 Phlyctenules are nodular inflammatory lesions
of the conjunctival, limbus or cornea
 Are commonly bilateral and primarily affects
children and young adults
When conjunctiva alone is involved symptoms are
relatively mild with itching, lacrimation and irritation
Corneal phlyctenules produce more severe symptoms -
FB sensation, photophobia, blepharospasm and
lacrimation

61.  Conjunctival and limbal phlyctenules are localized areas
of hyperemia with a nodular thickening in the centre;
later becomes necrotic and ulcerated. Resolution takes
place in 2-3 wks
 Corneal lesions initially resembles marginal keratitis and
are more severe , spread centrally and are associated
with vascularization
 Healing leaves characteristics triangular scars with the
base at limbus

62.  Phlyctenules are seen on microscopy to be
accumulation of lymphocytes: lesion represent cell-
mediated immune response in a previously
sensitized host
 Phlyctenulosis is commonly associated with
staphylococcal antigen but other causative antigens
include those derived from candida
spp, nematodes, lymphogranuloma venerum, adeno
virus and herpes simplex virus

63. Contact dermatoconjunctivitis
 An allergy that develops over a 48 hr period
following exposure to which there has been
previous sensitization
Contact sensitizing substances include locally applied
drugs esp atropine and neomycin, EDTA and
preservatives in ophthalmic preparations
(benzalkonium chloride, thiomersal), other sensitizing
substances include parabens (antimicrobial agents in
lotions, creams and cosmetics), lanolin
(medication, cosmetics) and p-phenylenediamine (hair
sprays, fabrics and shoes)
.

64.  Involves acute and chronic lesions of the
lids, conjunctiva and cornea
 Itching is a prominent symptom
Acute response comprises
injection and chemosis of
lower conjunctiva with the
serous or mucoid discharge
Papillae develop over the
entire conjunctiva
In chronic cases the lid
thickens and exhibit
dryness, fissuring and
crusting

65.  Associated kerathopy includes superficial
punctate epitheliopathy with erosion, sub
epithelial opacities, marginal
infiltration, ulceration and stromal edema in
severe cases
 The contact sensitizing substances are
generally haptens of low molecular weight that
bind to tissue proteins to form antigens
 Initial exposure sensitizes the immune system
and type IV hypersensitivity reaction ensues
48-72 hrs after exposure to the antigen

66. Type Immune-mechanism
Immediate (type
I)
hypersensitivity
Production of IgE antibody → immediate release of
vasoactive
amines and other mediators from mast cells; recruitment of
inflammatory cells (late-phase reaction)
Antibody
mediated (type II)
hypersensitivity
Production of IgG, IgM → binds to antigen on target cell or
tissue → phagocytosis or lysis of target cell by activated
complement or Fc receptors; recruitment of leukocytes
Immune
complex-
mediated (type
III)
hypersensitivity
Deposition of antigen-antibody complexes → complement
activation → recruitment of leukocytes by complement
products and Fc receptors → release of enzymes and other
toxic molecules
Cell-mediated
(type IV)
hypersensitivity
Activated T lymphocytes → i) release of cytokines and
macrophage activation; ii) T cell-mediated cytotoxicity

67. DIAGNOSTIC TESTING
 The diagnosis of ocular allergies is most often
made clinically, however special diagnostic
testing can be helpful in some cases.

68. Skin testing
 "skin-prick test“ provide supportive evidence
of allergies.
 also aid in identifying the specific allergen
causing the patient's problem and can be
helpful in avoiding the offending agent.
 test is sensitive for systemic allergies, but it is
positive in only 20% of patients with ocular
allergies

69.  During the test, allergens such as pollen, dust
mite extracts, or animal dander are applied to
the forearm or back by making shallow pricks
with a lancet or a needle.
 A skin wheal 2.0 mm or greater in diameter
occurring within 15 minutes of exposure is
considered a positive test result and indicates
that the patient is responsive to the allergen

70. Conjunctival provocation test
 In the conjunctival provocation test
(CPT), allergens are applied topically into the
conjunctival sac.
 presence of chemosis, hyperemia, and itching
within 20 minutes of instillation is considered a
positive response.

71. Biopsy of conjunctiva
 Cytology specimens can be obtained from the
conjunctiva, stained, and examined
microscopically for the presence of eosinophils
and mast cells.
 Eosinophils are not usually present in patients
without allergies but are present when an
allergic reaction is occurring.
Therefore, presence of eosinophils is
considered diagnostic of allergy.

72.  Eosinophils are present during the active
phase of VKC, but may be absent following
anti-allergy treatment or during the inactive
phase of VKC.
 presence of mast cells is also highly indicative
of active allergy

73. Tear fluid analysis
 A level of IgE in the tears greater than 16 iu/ml
is indicative of allergic conjunctivitis.
 Tryptase, histamine, leukotrienes, and certain
cytokines have also been found to be
increased in the tears of patients with ocular
allergies
 Analysis of the tears does not differentiate
between different types of ocular allergies.

74. MANAGEMENT OF OCULAR
ALLERGIES

75.  Treatment options for ocular allergies include
non-pharmacological and palliative
options, topical medications, oral
medications, and immunotherapy.
 The choice of treatment will depend on the
severity of the condition as well as medication
cost and expected patient compliance.

76. Non-pharmacological
treatment
 Non-pharmacological treatment including
allergen avoidance, cold compresses, and
artificial tears that provide short-term relief for
allergy symptoms.
 For example, avoidance of allergens can
result in up to a 30% decrease in symptoms..

77.  Avoiding allergens can involve some difficult
lifestyle changes such as removal of
pets, avoiding activities that patients enjoy, or
even moving to a location with different
environmental conditions.
 Use of cold compresses can reduce
vasodilatation and provide temporary
symptomatic relief.
 Artificial tears used 2 to 4 times daily can
also aid in removal and dilution of allergens
and can provide ocular lubrication.

78. Topical medications
 Topical medications provide ease of use, rapid
drug delivery and absorption, and decreased
systemic side-effects
 These medications act directly at the site of
application, e.g., the eyes, but ocular application
has also been shown to relieve nasal allergy
symptoms.
 It is thought that this occurs due to drainage of
the medication through the nasolacrimal duct to
the nose. Absorption through the nasal mucosa is
also responsible for producing systemic side-
effects.

79.  Vasoconstrictors, antihistamines, mast cell
stabilizers, non-steroidal anti-inflammatory
drugs (NSAIDs), and mild steroids are all
effective in managing ocular allergic
conjunctivitis.
 Each drug category acts at a different stage in
the inflammatory/allergy process.

80. Vasoconstrictors
 Vasoconstrictors are sympathomimetic
agents. Alone, they are effective at reducing
redness, but they have no direct effect on
the allergic response itself. For this reason,
these agents are often combined with an
antihistamines, which relieves itching.
 Adverse reactions to vasoconstrictors can
include burning and stinging on instillation
and mydriasis. Long-term use of topical
vasoconstricting agents is not
recommended due to the possibility of
rebound conjunctival hyperemia

81. Antihistamines
 Activation of H1 histamine receptors stimulate
itching, whereas H2 receptors are involved in
vasodilation.
 Topical ocular antihistamines bind to H1 receptors
in the conjunctiva and this reduces itching but
does not reduce redness.
 These medications do not affect other
proinflammatory mediators, such as
prostaglandins and leukotrienes
 topical antihistamines do not have a long duration
of action.
 Adverse reactions can include burning and
stinging on instillation, headache, and dry mouth.

82.  Levocabastine 0.05%
suspension, emedastine 0.05% solution
work primarily on H1 receptors.
 Emedastine is better at controlling itch and
redness than levocabastine.
 An antihistamine/vasoconstrictor drug
combination has been shown to be more
effective than either agent alone

83. Mast cell stabilizers
 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. Therefore, mast
cell stabilizers require a loading period of up to 2
weeks in order to achieve maximal efficacy.
 Mast cell stabilizers were originally approved for
treatment of chronic allergic conditions such as
GPC, AKC and VKC, but they have also been
found to be effective for treatment of SAC and
PAC.

84.  Cromolyn sodium 4% solution (first mast
cell stabilizer to be developed), Lodoxamide
0.1% solution, pemirolast 0.1%
solution, nedocromil 2% solution
 Lodoxamide has been shown to produce more
improvement in epithelial defects than
cromolyn sodium in conditions such as VKC
and AKC

85. Nonsteroidal anti-inflammatory
drugs
 NSAIDs inhibit prostaglandin production from
arachidonic acid by blocking cyclooxygenase.
In turn, this relieves itching and hyperemia.
 NSAIDs do not block other inflammatory
mediators, such as histamine.

86.  Topical NSAIDs provide good relief of ocular
itching and redness, but burning, conjunctival
chemosis, eyelid swelling, photophobia, and
foreign body sensation are not significantly
alleviated by these medications.
 Ketorolac 0.5% solution is currently the only
NSAID approved for the treatment of ocular
allergies

87. Corticosteroids
 Corticosteroids inhibit almost all inflammatory
mediators. They block the synthesis of new
histamine release by mast cells, inactivate
available histamine, inhibit mast cell
degranulation, decrease capillary
permeability, and inhibit phospholipase A
synthesis, which is used in the production of
arachidonic acid

88.  Topical steroids are often required to treat the
acute phase of severe forms of allergic
conjunctivitis, such as AKC, VKC, and GPC. Once
the condition is controlled, the steroid should be
tapered and treatment with mast cell stabilizers
and antihistamines should be used
 Patients using steroids, especially long-
term, should be monitored due to the potential for
side-effects, including increased intraocular
pressure (IOP), formation of posterior
subcapsular cataracts, and increased
susceptibility to ocular infection.

89. Topical immunosuppressive
agents
 Topical immunosuppressive agents are used
mainly as alternative therapies for patients who
have VKC or AKC. These agents inhibit
histamine degranulation, basophil
degranulation, T-lymphocyte
proliferation, cytokine production, and the
responsiveness of cells to cytokines.
 Cyclosporine 2% is a useful non steroidal anti
inflammatory and when used four times daily
has been shown to be safe and effective in
treating VKC when there is a concern about
side-effects associated with steroid use.

90.  Use of cyclosporine 2% allows patients to
safely reduce dependency on steroid use.
Blurred vision and stinging on instillation
are common side-effects of cyclosporine
2% use. Recently, cyclosporine 0.1%
ophthalmic solution has shown to be safe
and effective for treatment of VKC and
AKC.

91.  Tacrolimus is a potent immunosuppressive
macrolide.
 Topical 0.02% tacrolimus ointment is well
known to be effective in treating atopic
dermatitis.
 It has an immunosuppressive effect on T-
lymphocytes, B-lymphocytes and mast cells.
 Topical tacrolimus has been shown to be 30
times more effective than cyclosporine and is
an excellent and effective alternative, steroid-
sparing, treatment for severe GPC, AKC and

92.  Surgical treatment might be required in severe cases
of VKC and AKC, especially if corneal involvement is
present.
 These methods include removal of toxic substances at
the corneal ulcer site by scraping, superficial
keratectomy, or phototherapeutic keratectomy.
 Giant papillae can be removed by use of
cryotherapy, resection, or tarsectomy if they are
disrupting the corneal surface. Removal of giant
papillae decreases mechanical trauma, but this does
not appear to affect the immune process.
Therefore, the patient will need to continue the use of
mast cell stabilizers and antihistamines.

93. Finally…
 SAC and PAC are recurrent conditions, but
they can easily be controlled and do not
typically result in permanent visual loss.
Likewise, GPC also does not typically result in
permanent visual loss.
 On the other hand, VKC and AKC have sight-
threatening complications including corneal
ulcers and potential side-effects from the use
of steroid treatment.

94.  VKC will often subside following puberty, but
treatment might still be necessary later in life.
The prognosis for VKC patients is generally
good
 Unlike VKC, which often subsides
spontaneously at puberty, AKC is a persistent
problem that frequently results in decreased
visual function. The prognosis is guarded for
patients with AKC.

95.  Parents should be educated regarding the
recurrent and chronic nature of AKC.
Complications should also be explained.
 The use of sunglasses, hats with visors, and
swimming goggles will help patients avoid
non-specific triggers such as sun, wind and
dust.

96. REFERENCES
 Robbins Pathological basis of disease
 Section 8 - External Disease And Cornea –
AAO
 Clinical Ophthalmology - A Systematic
Approach - 7th Edition (2011) - Jack Kanski
 Clinical Ophthalmic Pathology-
 Management of Ocular Allergies - Denise
Goodwin, OD & Dina Erickson, OD, FAAO