Hira Nath DahalB. OptometryMaharajgunj Medical CampusInstitute of Medicine

OCULAR ALLERGY

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 hypersensitivityOcular allergy are a group of external

ocular conditions resulting from one or more types of hypersensitivity reactions to allergens

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

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

Type I hypersensitivity

Ig-E mediated hypersensitivity The sequence of events involved in type

I hypersensitivity reaction can be divided into three phases:

Sensitization phaseActivation phase(early

allergic response)Late allergic response

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

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

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

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

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

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)

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

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

Mediaters of allergicresponse

Mediator Activity Symptoms/Signs

Histamine Stimulate nerve endingsDilate blood vessels

ItchingRednessEdema

Platelet activating factor

Dilates blood vesselsEosinophil recruitment

Redness, edema

Leukotrienes/Prostaglandins

Dilates blood vesselsStimulate mucus production

RednessStringy mucus

Proteases May degrade small vessel basement membrane permeability

Swelling

Eosinophil chemotactic factor

Recruits eosinophils Prolong immune response

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)

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.

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 SAC and PAC

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.

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.

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

Bilateral intense itching is characteristic of VKC, but tearing, photophobia, blepharospasm, blurred 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

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

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

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

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

Limbal VKC:May develop alone or in association with

palpebral VKCLimbus has thickened, gelatinous

appearance with scattered opalescent mounds and vascular injection

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

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

These non-healing epithelial defects, also known as shield ulcers, are typically oval in shape and located superiorly.

Shield ulcer in vernal keratoconjunctivitis

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.

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.

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.

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

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.

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.

The signs of GPC consist ofhyperemia, thickening, and

abnormally large papillae (diameter >0.3 mm) on the superior tarsal conjunctiva

Giant papillary conjunctivitis

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

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.

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

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

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

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

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.

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

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.

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

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.

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

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

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

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

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 inflammationEqual amount of Ag and Ab produce moderate sized immune complexes and the inflammatory reaction is chronic but non-granulomatousExcess antigen results in small immune complexes which produce an acute vasculitis

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

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 lymphokinesTriggers a complex cellular response in which other lymphocytes, macrophages, fibroblasts and to a lesser extent , neutrophils are recruited and activated

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)

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

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 irritationCorneal phlyctenules produce more severe symptoms - FB sensation, photophobia, blepharospasm and lacrimation

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

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

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).

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 dischargePapillae develop over the entire conjunctiva

In chronic cases the lid thickens and exhibit dryness, fissuring and crusting

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

Type Immune-mechanism

Immediate (type I)hypersensitivity

Production of IgE antibody → immediate release of vasoactiveamines and other mediators from mast cells; recruitment ofinflammatory 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

DIAGNOSTIC TESTING

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

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

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

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.

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.

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

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.

MANAGEMENT OF OCULAR ALLERGIES

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.

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..

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.

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.

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.

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

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.

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

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.

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

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.

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

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

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.

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.

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.

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 VKC.

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.

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.

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.

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.

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