|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.
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. VKCs 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
An allergic response is an unwarranted over-reaction of the bodys
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 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
The bodys other defense mechanism, referred to as the arachidonic
acid cascade, produces three newly-formed inflammatory mediatorsprostaglandins,
thromboxanes and leukotrieneswhich 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 allergens 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
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
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 arachidonic by lipoxygenase. This leads to an interesting distinction in
anti-inflammatory treatment. Non-steroidal drugs prevent the formation of cyclooxygenase
but not lipoxygenase, thus they have virtually no effect on the production of
leukotrienes. As a result, non-steroidals are useful in reducing itching and conjunctival
injection but not very helpful in ridding the eye of excess immune cells. But because
steroids inhibit the production of arachidonic acid itself, they reduce the production of
all three eicosanoids. This is why we must use steroids to treat any inflammatory
conditions characterized by a build-up of immune cells, such as chalazia, uveitis or
VKC patients who present with shield ulcers also need aggressive
cycloplegia (atropine 1%, homatropine 5% or scopolamine 0.25%, b.i.d.) and a topical
antibiotic (Tobrex, Ciloxan Ocuflox or Polytrim) q4-6h. To reduce the interaction between
the lid and cornea, provide a low-water content soft lens as a bandage lens. When the
corneal lesion has re-epithelialized, begin topical steroid therapy.
Newer anti-histamines, such as dual-action olopatadine hydrochloride
0.1% (Patanol) b.i.d. as well as emedastine difumarate 0.5% (Emadine) q.i.d. have been
seen to be very effective. A recently developed steroid, loteprednol etabonate (Alrex)
q.i.d. is specifically marketed for the management of allergic conjunctivitis.
Other reports in this section
Allergic Conjunctivitis &Vernal Keratoconjunctivitis
Chlamydial & Gonococcal Conjunctivitis
Superior Limbic Keratoconjunctivitis (SLK of
Conjunctivitis with Pseudomembrane
Giant Papillary Conjunctivitis
- Educate patients with a history of seasonal allergic conjunctivitis about
how to avoid exposure to substances that precipitate symptoms, and recommend prophylactic
treatment with a mast cell stabilizer. If effective, maintain this therapy for the
duration of the season.
- Follow-up with patients on non-steroidal medicines in one to two weeks
after the start of therapy. See patients on topical steroids no later than one week after
the start of therapy, and monitor their IOP routinely for the duration of the therapy.
Re-examine patients treated for shield ulceration every one to three days.
- Mast cell degranulation only occurs in allergic reactions, but the
arachidonic acid cascade occurs after any threatening event, such as bacterial infection,
surgery or accidental trauma.
- Follow up with patients placed on topical medications after one week,
with close monitoring thereafter.
Mild Allergic Reaction
Severe Allergic Reaction