Allergic conjunctivitis is an inflammatory response of the conjunctiva to an allergen. It is part of a larger systemic atopic reaction and is usually seasonal with associated upper respiratory tract symptoms and complaints of redness and swelling of the conjunctiva with severe itching and increased lacrimation. Presence of rhinitis often terms this process as allergic rhinoconjunctivitis.
372.00 Acute conjunctivitis, unspecified
372.05 Acute atopic conjunctivitis
372.1 Chronic conjunctivitis
372.10 Chronic conjunctivitis, unspecificied
372.13 Vernal conjunctivitis
372.14 Other chronic allergic conjunctivitis
H10.1 Acute atopic conjunctivitis
H10.10 - unspecified eye
H10.11 - right eye
H10.12 - left eye
H10.13 - bilateral
H10.4 Chronic conjunctivitis
H10.40 Unspecified chronic conjunctivitis
H10.401 right eye
H10.402 left eye
H10.409 unspecified eye
H10.41 Chronic giant papillary conjunctivitis
H10.411 right eye
H10.412 left eye
H10.419 unspecified eye
H10.44 Vernal conjunctivitis
H10.45 Other chronic allergic conjunctivitis
- Vernal - of, or appropriate to spring
- Atopic - denoting a form of allergy or hypersensitivity reaction
- Perennial - chronic, year round
- Allergic conjunctivitis
- without involvement of the cornea:
- Symptom duration ~24 hours - acute allergic conjunctivitis
- Symptoms occurring during one season - seasonal allergic conjunctivitis (SAC)
- Symptoms occurring throughout all seasons - perennial allergic conjunctivitis (PAC)
- with involvement of the cornea:
- Vernal keratoconjunctivitis (VKC)
- Atopic keratoconjunctivitis (AKC)
- without involvement of the cornea:
Allergic conjunctivitis is one of the most common forms of conjunctivitis. In a report from the National Health and Nutrition Examination Survey studying the epidemiology of allergic conjunctivitis, 6.4% and 29.7% of 20,010 patients reported ocular symptoms and combined ocular and nasal symptoms, respectively. 40% of the population reported experiencing at least 1 occurrence of ocular symptoms in the past 12 months.
Atopic keratoconjunctivitis occurs predominantly between the late teenage years and fifth decade of life. It relapses and remits with no seasonal correlation. Atopic dermatitis is present in 95% of cases and asthma in 87% of cases. 
Vernal keratoconjunctivitis changes with the seasons. Commonly seen in prepubescent males ranging from age 5-20 with a peak incidence at 11-13. Males are twice as often affected than females. More often seen in warm, dry, climates with a decrease in inflammation and symptoms in the winter. 
Without corneal involvement
|Environmental allergens, particularly if they are known; an example is cat dander.|
|Environmental allergens that are often associated with changes in seasons; examples include grass and weed pollens.|
|Environmental allergens that occur throughout the year; examples include Indoor allergens: dust mites, mold, animal dander.|
With corneal involvement
|Environmental allergens may incite an acute exacerbation. Most commonly present during the springtime with the associated increase in pollen. Increased presence in hot and dry environments with a decrease in inflammation and symptoms during the winter months.|
|Genetic predisposition to atopic reactions with comorbid asthma and atopic dermatitis commonly present. Increased risk with positive family history. Environmental allergens may cause an acute exacerbation as well. No changes with seasons.|
Giant papillary conjunctivitis (GPC)
|Commonly seen in individuals wearing soft contact lens who infrequently replace their lenses, wear their lenses for prolonged periods of time, have poor lens hygiene, have poor contact lens fitting, or are allergic to the various contact lens solution. Similarly, irritation from exposed sutures or prostheses increase the risk for developing GPC.|
Seasonal and perennial allergic conjunctivitis
The general idea is that there is an allergic response in the conjunctivitis to an allergen. The allergen causes cross-linkage of membrane-bound IgE that causes mast cells to degranulate. This causes a release and cascade of allergic and inflammatory mediators, such as histamine. 
Vernal keratoconjunctivitis and atopic keratoconjunctivitis
The pathophysiological mechanism of disease is not fully understood. However, evidence suggest the involvement of various cells within the conjunctiva, specifically eosinophils, fibroblasts, epithelial cells, mast cells, and TH2 lymphocytes. Allergens activate these various cells creating an inflammatory response. 
Giant papillary conjunctivitis
This is not a true ocular allergy but rather an repetitive mechanical irritation, often in due to contact lenses, that is aggravated by concomitant allergy. 
Removal of allergen, such as pollen or stitches.
The diagnosis is clinical based on history, signs and symptoms, and physical exam findings. An allergy panel for identification of specific allergen can be considered. In addition, confocal microscopy can be used to evaluate some forms of allergic conjunctivitis, such as atopic conjunctivitis.
Signs and Symptoms
Itching is the primary symptom where patients are constantly rubbing their eyes with temporary relief. The eyelids and conjunctiva become edematous and diffusely hyperemic. Presentation is most often bilateral, due to the systemic nature of the disease.
|Type of Allergic Conjunctivitis||Physical Exam Findings|
|Bilateral conjunctival injection, chemosis, watery discharge, and mild mucous discharge.|
Vernal keratoconjunctivitis (VKC)
|Bilateral bulbar conjunctival injection with associated watery and mucoid discharge. Patients develop a giant papillary hypertrophy of only the superior tarsal conjunctiva, resembling “cobblestones”. Specific findings that help differentiate VKC from AKC are: limbal (Horner-Trantas) dots which are small white-yellow chalky concretions around the corneal limbus; corneal vernal plaques; or shield (Togby’s) shaped ulcers of the cornea. Just as in AKC, patients, if untreated, can develop conjunctival scarring or corneal neovascularization, scarring, or erosions/ulcers.|
Atopic keratoconjunctivits (AKC)
|Bilateral conjunctival injection with associated eczematoid belpharitis, watery/mucoid discharge, and boggy edema. Papillary hypertrophy of superior or inferior tarsal conjunctival can occur with increased risk for eyelid thickening and scarring. In more severe and untreated cases, patients can develop loss of eyelashes, conjunctival scarring, corneal neovascularization, ulcers or scars, punctate epithelial keratitis and associated keratoconus and/or anterior/posterior subcapsular cataracts.|
Giant papillary conjunctivitis (GPC)
|The laterality of symptoms is associated with contact lens, suture, or prostheses wear pattern. Most notably, patients will have papillary hypertrophy of the superior tarsal conjunctiva. In long-standing, untreated disease, the papillae will develop white fibrotic centers. In severe cases, patients will have lid swelling and ptosis.|
|Allergic conjunctivitis||Natural History||Potential Sequelae|
|Seasonal/Perennial conjunctivitis||Recur seasonally with the changes in pollens and allergens present.||Minimal or local inflammation that often resolves and remits.|
|Vernal keratoconjunctivitis (VKC)||The onset of symptomatology begins in childhood and peaks at about 11-13 with acute exacerbations occurring more frequently during the spring and summer months. Commonly patients will “grow out” of the disease with decreased symptoms ranging from 2-30 years of age.||Untreated VKC can lead to eyelid thickening that ultimately leads to ptosis. Severe corneal involvement can cause corneal neovascularization, thinning, ulceration, and infection. This can lead to vision loss or development of keratoconus. Conjunctival scarring can also occur.|
|Similar to VKC, the onset of symptoms occurs during childhood but peaks during young adult and continues into the fifth decade of life. The course remains chronic with periodic acute exacerbations.||The natural sequelae is similar to VKC with eyelid thickening or tightening. Conjunctival scarring can occur and involvement of the cornea can lead to scarring, neovascularization, thinning, ulceration and infection. This can also develop into keratoconus or cause vision loss. There can also be development of concurrent anterior or posterior subcapsular cataracts.|
|Giant papillary conjunctivitis (GPC)||This disease process is directly correlated with presence of risk factors. Therefore, continued contact lens wear, exposed corneal or scleral sutures, or ocular prosthesis cause worsening or increasing in symptoms.||If left untreated, GPC can cause acquired ptosis.|
- Infectious conjunctivitis
- Dry Eyes Syndrome
- Toxic conjunctivitis
- Ocular rosacea
- Angle Closure glaucoma
- Phlyctenular conjunctivitis
Seasonal/Perennial Allergic Conjunctivitis
Topical drops for allergic conjunctivitis come in many different forms. Here we outline a general overview/suggestions of the different options. Of note, chronic use of vasoconstrictive agents can lead to rebound vasodilation when discontinued.
- First line: Over-the-counter antihistamine/vasoconstrictor agent. Vasoconstrictors: Inexpensive over-the counter are first line. Many brands are available containing antazoline phosphate 0.05%, naphazoline HCl 0.05%, oxymetazoline HCl, tetrahydrozoline HCl 0.05%, or phenylephrine 0.12%.
- Second line: Second-generation topical histamine H1-receptor antagonist. H-1 receptor antagonists: More effective than the vasoconstrictors, but much more expensive. The three principal choices are pheniramine maleate 0.3% (Naphcon), emedastine (Emadine), and levocabastine HCl 0.05% (Livostin)
- Third line: recurrent/persistent - mast-cell stabilizers can be used. Mast cell stabilizers: cromolyn sodium 4% (Crolom), nedocromil 2% (Alocril), pemirolast 0.1% (Alamast), and lodoxamide tromethamine 0.1% (Alomide). These are FDA-approved only for a specifically vernal conjunctivitis. Use only if other classes of medications have failed.
- Combined medications can also be used: Combined H-1 receptor antagonist and mast cell stabilizers: olopatadine hydrochloride 0.1% (Patanol), optivar, ketotifen (Zaditor), and Elestat. These agents are more effective than the mast cell stabilizers alone.
- If symptoms are not adequately controlled: Brief course of low-potency and low-frequency topical corticosteroids. NSAID such as ketorolac has been approved by FDA for use of seasonal allergic conjunctivitis but are generally used as adjunctive agents. Nonsteroidal anti-inflammatory agents: ketorolac tromethamine 0.5% (Acular).
- Oral antihistamines, such as Xyzal (levocetirizine), Zyrtec (cetirizine), Allegra (fexofenadine), Clarinex (desloratadine) and Clarinex (loratadine), can be used, especially if the patient is experiencing additional systemic effects.
- Some additional measures can be used as adjunctive measures to improve symptom management are as follows:
- Artificial tears to dilute allergens
- Cool compresses / ice packs
- Avoid Allergens
- Frequent clothes washing and bathing/showering before bedtime
- Refer/consult allergy or dermatology for those who are not adequately controlled with topical medications and oral antihistamines
Although the disease process is more advanced in both VKC and AKC, the general treatment strategies remain similar to management of seasonal or perennial allergic conjunctivitis. If, however, an acute exacerbation occurs, topical corticosteroids are often added to reduce inflammation. Another adjunctive therapy is addition of topical cyclosporin 2%. If the VKC or AKC is not responsive to topical therapy, supratarsal injection of corticosteroid can be considered.
Giant Papillary Conjunctivitis
The most important management in GPC is modifying the causative entity. This generally includes removal or replacement of sutures, rotating the knots, or using a therapeutic contact lens.
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- Boyd K, Pagan-Duran B. Giant Papillary Conjunctivitis. American Academy of Ophthalmology. EyeSmart® Eye health. https://www.aao.org/eye-health/diseases/giant-papillary-conjunctivitis-list. Accessed March 22, 2019.
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- Ocular Pathology Atlas. American Academy of Ophthalmology Web site. https://www.aao.org/resident-course/pathology-atlas. Published 2016. Accessed January 4, 2017.