SIGNS AND SYMPTOMS
Itching and conjunctival injection are the two hallmarks of an allergic reaction. Also definitive is a lack of palpable preauricular lymph nodes, since palpable preauricular nodes signify viral infection. The eyelids may be swollen and red, and you may also see papillae of the palpebral conjunctiva. In most cases, patients will report a history of seasonal or other allergies.
Seasonal allergies typically produce a thin, watery discharge and do not involve the cornea. If the patient exhibits thick, ropy discharge with severe itching and corneal involvement, it is most likely VKC rather than a seasonal allergy. VKC’s prevalence is higher in the warmer climates. Onset is typically between the ages of three and 25 years. Males are typically more affected than females.
The important clinical signs of VKC include large conjunctival papillae on the back of the superior tarsus, Horner-Trantas dots (gelatinous, white clumps of degenerated eosinophils at the superior limbus), areas of superficial punctate keratitis (SPK) and, in severe cases, well demarcated, sterile, superiorly located corneal shield ulcers.
An allergic response is an unwarranted over-reaction of the body’s immune system to foreign substances known as allergens, which the body wrongly perceives as a potential threat. The response can be innate or acquired. The presence of an allergen on the conjunctiva initiates two simultaneous immune responses, one caused by the release of so-called “pre-formed” inflammatory mediators such as histamine from mast cells, and the other by the production of arachidonic acid and its conversion into so-called “newly-formed” mediators such as prostaglandins (see “Tracing the Complex Path of Allergic Reactions,” on next page). Pre-formed mediators are released immediately upon exposure; newly-formed mediators are delayed roughly eight to 24 hours.
In mast cell degranulation, the allergen attracts and binds to an antibody known as immunoglobulin E (abbreviated as “IgE”), then adheres to mast cells and causes them to degranulate, like a key opening a lock. This discharges the pre-formed mediators. Their effects can be either direct, indirect or a combination of the two.
Two important mediators released from mast cells, histamine and bradykinin, immediately begin to stimulate nerve endings called nociceptors, creating the sensation of itching. Both also increase vascular permeability and vasodilation; this causes the clinical signs of redness and conjunctival injection.
Meanwhile, other mediators released from mast cells send out chemical signals that attract both red and white blood cells to the area. Once these cells arrive, they easily reach the conjunctival surface by moving through the dilated and highly permeable capillaries.
The body’s other defense mechanism, referred to as the arachidonic acid cascade, produces three newly-formed inflammatory mediators—prostaglandins, thromboxanes and leukotrienes—which are collectively known as eicosanoids.
Virtually all cells contain a phospholipid layer within their cell walls. Any disruption or threat signals the cell to convert phospholipids into arachidonic acid. When arachidonic acid interacts with two enzymes known as cyclooxygenase and lipoxygenase, it is metabolized into eicosanoids. An allergen’s presence initiates the arachidonic acid cascade both within conjunctival epithelial cells and also within mast cells as they degranulate.
Much like histamine and bradykinin, prostaglandins directly stimulate nerve endings to produce sensations of itching and pain, and also increase vascular permeability and vasodilation. Leukotrienes primarily attract macrophages (white blood cells).
Management of both allergic conjunctivitis and VKC is primarily aimed at alleviating symptoms. The most effective but least practical treatment is to prevent exposure to the allergen. Since this is not usually possible, instruct patients to frequently use cold compresses, artificial tears and ointments to soothe, lubricate and wash away the allergens. Also recommend that patients use a topical decongestant such as naphazoline or phenylephrine as needed. These drugs cause vasoconstriction, retarding the release of the chemical mediators into the tissues from the blood stream. This reduces hyperemia, chemosis and other symptoms.
Mast cell stabilizers such as Alomide and Crolom help prevent the onset of allergic reactions by blocking the adherence of the IgE-allergen compound to the mast cell. Treat patients with a history of recurrent seasonal allergies using a mast cell stabilizer q.i.d. for four weeks in advance of allergy season. Patanol (olopatadine 0.1%) combines mast cell stabilization with an antihistamine to offer therapy that is for both acute and chronic symptoms. The effects last eight hours, allowing for b.i.d. rather than q.i.d. dosing.
In moderate to severe cases, recommend one or more of the following, used from two to four times per day as needed: a topical medication such as Patanol or Livostin, oral antihistamines such as Benadryl, or a topical non-steroidal anti-inflammatory drug (Acular, Voltaren or Profenal). In extremely symptomatic cases, use a topical steroid such as Vexol, Flarex or Alrex q.i.d.
Only prostaglandins and thromboxanes are produced when cyclooxygenase interacts with arachidonic acid. Leukotrienes, by contrast, are produced from the break-down of arachido