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Thursday, December 23, 2010

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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