| Toxic Conjunctivitis Signs and Symptoms
Toxic conjunctivitis, sometimes referred to as toxic follicular
conjunctivitis, is a syndrome that results when the palpebral and bulbar conjunctiva have
been chronically exposed to any number or combinations of foreign substances. The process
may occur unilaterally or bilaterally, depending upon exposure. Its clinical features
include the presentation of ocular itching, burning and tearing, injection of the bulbar
and palpebral conjunctivae, chemosis, along with inferior and or superior eyelid follicle
and papillae formation, and an absence of preauricular lymphadenopathy. Keratopathy is
often present secondarily. In chronic cases, pannus formation may result.
Typically, patients present with a history of using or starting an
ocular medication for an episode of presumed bacterial or viral conjunctivitis only to
find that the ocular symptoms and signs continue to increase despite correct usage of the
medicine. The term medicamentosa is applicable here; it connotes a reaction to the
preservatives in medications, or the medications themselves, producing a more substantial
keratitis.
Pathophysiology
The toxic/allergic response is an over-reaction of the body’s immune
system to immunogens or allergens. The response can be innate or acquired. A variation of
this over-reaction is manifested when the body responds hyperactively to exogenous
materials such as medicines, contact lenses, contact lens solutions, dust, dander or viral
shedding. Overactivity of this type is commonly referred to as a toxic or allergic
reaction. With respect to the eye and its adnexa, the result is toxic conjunctivitis.
The key component to the ocular allergic response is the mast cell. When
mast cells interact with specific allergens, like a lock being opened by a key, they open
(degranulation) discharging chemical mediators into the surrounding tissues. The primary
chemical mediators include histamine (responsible for increased vascular permeability,
vasodilation, bronchial constriction and increased secretion of mucous), neutral proteases
(generating other inflammatory mediators) and arachidonic acid (crucial component of the
cyclooxygenase pathway leading to production of prostaglandins and leukotrienes).
There are four types of hypersensitivity reactions.
Type I reactions are immediate hypersensitivity reactions
or anaphylactic reactions. These reactions produce sudden degranulation of mast cells
mediated by the antibody IgE.
Type II reactions involve the body’s ability to
distinguish itself from non-self. Abnormalities in this element of the system give rise to
autoimmune disease.
Type III reactions involve combinations of antigen and
antibody known as immune complexes. Offending triggers may be intrinsic (i.e. a protein
molecule) or extrinsic (a penicillin molecule) and produce a significant tissue response
in an attempt to rid the area of the invader.
Type IV reactions, sometimes referred to as cell mediated
hypersensitivity reactions, involve the T-lymphocytes and lymphokines. The reaction is
classically delayed until sufficient antigens stimulate the chemical cascade. In the
ocular tissues, these chemical exchanges incite conjunctival and adnexal vasodilation,
chemosis, edema and lacrimation. Individuals experience pain, itching, swelling and
irritation. The discharge produced is typically serous and the conjunctival findings
include follicles (hyperplasia of lymphoid tissue within the eyelid stroma) and papillae
(hyperplastic palpebral conjunctival epithelium infiltrated by lymphocytes and plasma
cells).
Management
Management is primarily aimed at reducing symptomatology. Cold compress,
artificial tear drops and ointments soothe and lubricate. Topical decongestants produce
vasoconstriction, reducing hyperemia, chemosis and other symptoms by retarding the release
of the chemical mediators into the tissues from the blood stream. Topical antihistamines
(Emadine, Livostin, b.i.d. to q.i.d.) and oral antihistamines (Benadryl, 25 to 50mg, p.o.
t.i.d.) are also excellent therapies for acute signs and symptoms. Mast cell stabilizers
such as cromolyn sodium (Opticrom) and lodoxamide tromethamine (Alomide) may be useful in
seasonal or chronic cases. The non-steroidal anti-inflammatory drugs (NSAIDS: Acular,
Voltaren, b.i.d. to q.i.d.) may offer relief in moderate cases, while topical steroid
preparations (Alrex, Lotemax, FML, FML Forte, Allergan, Pred Mild, Pred Forte, Flarex,
Vexol, b.i.d. to q.i.d., and Inflamase Mild and Forte, b.i.d. to q.i.d.) are reserved for
the most symptomatic presentations.
Clinical Pearls
Toxic/allergic conjunctivitis is a diagnosis that can be
made based upon history and course. Typically, vision is unaffected despite its unruly
appearance. You can usually identify a causative source as the precipitator of the acute
signs and symptoms. Even if left untreated, toxic conjunctivitis often begins to resolve
within seven days.
In true toxic conjunctivitis, there will not be a
palpable preauricular lymph node.
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