Infiltrative keratitis

Abuse of topically administered drugs by practitioners or patients can cause significant ocular toxicity. Infiltrative keratitis has occurred from long-term use of anesthetic eyedrops for relief of pain associated with corneal abrasions. Bilateral posterior subcapsular cataracts have developed after the topical administration of prednisolone acetate 0.12% twice daily over long durations. Practitioners should closely monitor patients treated with drugs known to have potentially significant ocular or systemic side effects. 

When evaluating an acute injmy of the cornea, the practitioner is sometimes tempted to prescribe a topical anesthetic for administration at home by the patient for relief of ocular pain. This practice is extremely dangerous, however, and in numerous instances has led to severe infiltrative keratitis and even loss of the eye from anesthetic misuse or abuse by the patient.Topical anesthetics must be used only for the pmpose of obtaining initial relief of ocular pain and never as part of a prolonged therapeutic regimen.The potential corneal toxicity of topical anesthetics precludes their use as self-administered drugs. 

Infiltrative events includes six subcategories microbial keratitis, CL-induced peripheral ulcer, CL-induced red eye, infiltrative keratitis, asymptomatic infiltrative keratitis, and asymptomatic infiltration... 

It is also important to differentiate a red eye associated with contact lens wear from other potential causes. The definitive diagnosis can pose a clinical challenge with respect to excluding other conditions that cause an acute red eye with corneal infiltration. EKC, chlamydial keratoconjunctivitis, marginal infiltrative keratitis,... 

Figure 26-59 An anterior stromal scar remains farrow ) after resolution of infiltrative keratitis and associated comeal infiltrate.

Culture if keratitis is severe or sight-threatening. Otherwise, cultures or smears are used only if the corneal infiltrate is chronic or unresponsive to broad-spectrum antimicrobial therapy.19... 

Ciprofloxacin White crystalline precipitates lid margin crusting crystals/scales foreign body sensation itching conjunctival hyperemia bad taste in mouth corneal staining keratopathy/keratitis allergic reactions lid edema tearing photophobia corneal infiltrates nausea decreased vision. 

Immune reaction after keratoplasty Herpes zoster keratitis Disciform keratitis Marginal corneal infiltrates Superficial punctate keratitis Chemical burns Acne rosacea keratitis Interstitial keratitis Uvea... 

Epidemic keratoconjunctivitis Pharyngoconjunctival fever Any age Predominandy children Follicles, hyperemic membranes Follicles, hyperemic membranes Subepithelial infiltrates common Superficial punctate keratitis subepithelial infiltrates not common Tender, palpable preauricular node Fever, pharyngitis, nontender node Adenovirus types 8 and 19 Adenovirus types 3 and 7... 

In its early stages trachoma presents as a chronic follicular conjunctivitis with a predilection for the superior tarsal and bulbar conjunctiva. Over time, the conjunctival reaction becomes papillary in nature and, with the inflammatory infiltration that occurs, the follicular character of the infection can become obscured. Patients experience symptoms of photophobia, tearing, and mucoid or mucopurulent discharge. Limbal edema and superior bulbar conjunctival hyperemia also may occur. Conjunctival follicles that form at the limbus are characteristic of severe trachoma. Primary corneal involvement often includes superior epithelial keratitis and superficial superior pannus formation. A wide variety of corneal infiltrates... 

During the examination, and when considering the history of the traumatic episode, it is important to rule out corneal laceration or penetration, retained foreign bodies, or other ocular traumatic sequelae. Clean corneal abrasions should not exhibit opaque infiltration suggestive of bacterial or fungal keratitis. 

Unlike dendritic keratitis, indolent ulcers are typically very difficult to treat. Instillation of a prophylactic antibiotic, such as polymyxin B-bacitracin ointment two to four times a day, and a cycloplegic agent, such as 5% homatropine two to three times a day, is indicated. Therapeutic soft contact lens use with appropriate antibiotic therapy can also be considered as alternatives. These patients must be monitored carefully to ensure that no secondary infection develops. If the ulcer deepens, a new infiltrate forms, or if there is an increase in the anterior chamber reaction while the patient is being treated, cultures should be performed to rule out bacterial or fungal infection. Cyanoacrylate glue, conjunctival flap surgery, or tarsorrhaphy may be required if healing does not occur. 

Deep corneal edema with folds in Descemet s membrane, in the presence of an intact epithelium, can develop from 3 to 4 months after acute HZO. This disciform keratitis may involve the full thickness of the cornea and may be surrounded by a ring-like cellular infiltrate called a Wessley ring. It is considered to be an immune response to viral antigens and responds quickly to topical steroids, especially when initiated early. Unfortunately, it is common to have recurrences when steroids are tapered or discontinued and can lead to corneal scarring or, more seriously, corneal melt.There is often an associated anterior uveitis with keratic precipitates as well as diffuse corneal edema, endothelial cell loss, and increased lOP secondary to trabeculitis. 

TSPK is a chronic epithelial keratitis of unknown etiology, suggested to be due to chronic subclinical viral infection in the deep layers of the basal epithelium. Support for this theory includes the protracted coruse of this condition, its tendency to recur, the lack of effect by antibiotics on its clinical course, and lack of bacterial isolation from eyes affected by the condition. The clinical presentation of corneal mononuclear cell infiltrates, the rapid resolution of these infiltrates with topical steroids, and their rapid reappearance if topical steroids are stopped too quickly support the possibility that the primary presentation is a typical immunologic response. 

Figure 26-53 Acanthamoeba keratitis. ( 4) Active infection. (B) Ring-infiltrative pattern of late-stage infection.

Clinical signs of Acanthamoeba keratitis include lid edema, conjunctival injection, and usually a fluctuating anterior chamber reaction. Early in the disease course an edematous necrotic dendritiform keratitis, central or paracentral infiltration, or elevated epithelial lines may be evident. Late in the course a prominent complete or partial stromal ring-shaped infiltrate with recurrent epithelial breakdown is highly suggestive of this... 

A 68-year-old woman developed bilateral marginal keratitis 2 weeks after starting to use dorzolamide eye-drops (9). One week after withdrawal she was asymptomatic, with complete resolution of her corneal infiltrates. 

Mustard initially causes vasodilation and increased vascular permeability in the conjunctiva, which lead to progressive edema. Secretion of mucus occurs within minutes of exposure. Pyknosis of epithelial cells begins concurrently with or shortly after these changes, leading to desquamation of the epithelium. In the later stages, inflammatory infiltration of connective tissue and exudation are present (Warthin and Weller, 1919 Maumenee and Scholz, 1948). Medical personnel have reported seeing delayed keratitis in humans from as little as 8 months to 20 years after mustard exposure (Mann and Pullinger, 1944 Atkinson, 1948). This delayed keratitis, in addition to the chronic inflammation, can lead to erosions and frank ulcerations. 

---