Allergic Conjunctivitis Clinical Presentation

Updated: Jun 08, 2017
  • Author: Mark Ventocilla, OD, FAAO; Chief Editor: Andrew A Dahl, MD, FACS  more...
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Diagnosis of allergic conjunctivitis generally is made by taking a thorough history and by careful clinical observation. In seasonal and perennial allergic conjunctivitis, important features of the history include a personal or family history of atopic disease, such as allergic rhinitis, bronchial asthma, and/or atopic dermatitis. Perhaps the most important feature in the clinical history is the symptom of itching. Without itching, the diagnosis of allergic conjunctivitis becomes suspect.

Vernal keratoconjunctivitis

With vernal keratoconjunctivitis (VKC), as with other allergic or type I hypersensitivity disorders, itching is the most important and most common symptom. Other commonly reported symptoms are photophobia, foreign body sensation, tearing, and blepharospasm. Photophobia due to chronic keratitis is also common.

Ocular signs of VKC commonly are seen in the cornea and conjunctiva. In contrast to atopic keratoconjunctivitis (AKC), the eyelid skin usually is not as significantly involved.

Atopic keratoconjunctivitis

In AKC, unlike VKC, the symptoms are perennial. There may be seasonal variation, however, with worsening symptoms during winter months. The single most common symptom is bilateral itching of the eyelids, but watery discharge, redness, photophobia, and pain may be associated.

Giant papillary conjunctivitis

Primary symptoms in giant papillary conjunctivitis (GPC) are ocular itching with a mucoid or ropy discharge, very similar to that seen in VKC. Another symptom of GPC may be persistent foreign body sensations when using contact lenses, resulting in a decrease wear time and potential reduction in the visual acuity. Contact lens intolerance is especially problematic in patients with keratoconus who are highly dependent on contact lenses for optimal visual function.


Physical Examination

Seasonal and perennial allergic conjunctivitis

Classic signs of allergic conjunctivitis include injection of the conjunctival vessels as well as varying degrees of chemosis (conjunctival edema) and eyelid edema. The conjunctiva often has a milky appearance due to obscuration of superficial blood vessels by edema within the substantia propria of the conjunctiva. Edema is generally believed to be the direct result of increased vascular permeability caused by release of histamine from conjunctival mast cells.

Vernal keratoconjunctivitis

VKC may be subdivided into 2 varieties, as follows: palpebral and limbal. The classic conjunctival sign in palpebral VKC is the presence of giant papillae. The papillae most commonly occur on the superior tarsal conjunctiva; usually, the inferior tarsal conjunctiva is unaffected. Giant papillae assume a flattop appearance, which often is described as "cobblestone papillae." In severe cases, large papillae may cause mechanical ptosis (drooping eyelid). The astute clinician's attention is always drawn to the everted upper tarsus, which reveals key telltale signs, including papillae, vascular abnormalities, conjunctival inclusion cysts, follicles, subconjunctival scarring, and entropion.

A ropy mucous discharge may be present, which commonly is associated with tarsal papillae. Large numbers of eosinophils, indicating the presence of extended periods of inflammation, are present in the discharge.

The limbal form of VKC commonly occurs in dark-skinned individuals, such as those from Africa or India. As the name implies, papillae tend to occur at the limbus, the junction between the cornea and the conjunctiva, and have a thick gelatinous appearance. They commonly are associated with multiple white spots (Horner-Trantas dots), which are collections of degenerated epithelial cells and eosinophils. Horner-Trantas dots rarely last longer than a week from their initial presentation and generally resolve rapidly with the initiation of topical corticosteroid therapy.

While corneal vascularization is rare, the cornea may be affected in a variety of ways. Punctate epithelial keratopathy (PEK) may result from the toxic effect of inflammatory mediators released from the conjunctiva. The appearance of PEK may be a precursor for the characteristic shield ulcer, which is pathognomonic of VKC. PEK can coalesce, resulting in frank epithelial erosion and forming into a shield ulcer, which is typically shallow with white irregular epithelial borders.

Although the pathogenesis of a shield ulcer is not well understood, the major factor in promoting development may be chronic mechanical irritation from the giant tarsal papillae. Some evidence suggests that the major basic protein released from eosinophils may also promote ulceration.

Another type of corneal involvement is vernal pseudogerontoxon, which is a degenerative lesion in the peripheral cornea resembling corneal arcus. Keratoconus may be seen in chronic cases, which may be associated with chronic eye rubbing in predisposed individuals.

Atopic keratoconjunctivitis

AKC may affect eyelid skin and lid margin, conjunctiva, cornea, and lens. Skin of the eyelids may exhibit eczematoid dermatitis with dry, scaly, and inflamed skin and the lid margins may show meibomian gland dysfunction and keratinization. Moreover, staphylococcal colonization of eyelid margins is very common in AKC and may result in blepharitis. Conjunctiva may show chemosis and typically a papillary reaction, which is more prominent in the inferior tarsal conjunctiva, in contrast to that seen in vernal keratoconjunctivitis.

Hyperplasia of limbal regions may result in a gelatinous thickening, similar to the limbal variant of VKC, and, although rare, Horner-Trantas dots also may be present. Fibrosis or scarring of the conjunctiva may result in a shortened fornix or symblepharon formation with chronic inflammation. Corneal involvement ranges from PEK early in the course of the disease, to neovascularization, stromal scarring, and possibly ulceration. There is also a strong association between AKC and herpes simplex labialis and herpes simplex viral keratitis.

As seen in VKC patients, the chronic eye rubbing of the cornea may contribute to the development of keratoconus. Characteristic lenticular changes in AKC include anterior or posterior subcapsular cataract formation. These slow progressing lens opacities are usually bilateral and present in the second decade of life. There is some reasonable speculation that the long-term use of topical corticosteroids can also induce the lenticular changes later in life.

Giant papillary conjunctivitis

Examination of superior tarsal conjunctiva reveals the presence of large cobblestone papillae, which are generally 0.3 mm or greater in diameter.

In her original description of GPC in 1977, Allansmith described 3 zones of superior tarsal conjunctiva. [3] Zone 1 is located closest to the fornix and is the most inferior portion of the tarsal conjunctiva seen when the upper eyelid is everted. Zone 3 is located closest to the eyelid margin. Zone 2 is located between zone 1 and zone 3.

Papillae typically associated with soft contact lenses initially appear in zone 1 and progress toward zone 3, while those associated with rigid gas permeable contact lenses exhibit a reverse pattern, with zone 3 affected first. GPC associated with a localized irritant, such as an exposed suture or a filtering bleb, is typically localized to the area overlying these inciting lesions.

Another clinical sign of GPC may be chronic bulbar conjunctival injection and inflammation due to prolonged and persistent use of contact lenses.