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Eosinophilic keratitis — Clinical Guidelines

Overview

Eosinophilic keratitis is a condition characterized by the infiltration of eosinophils into the corneal stroma, leading to inflammation and potential visual impairment. This condition primarily affects individuals with atopic dermatitis, asthma, or other eosinophil-related disorders, making it particularly relevant in patients with a history of atopy. Clinicians must recognize eosinophilic keratitis early to prevent complications such as corneal scarring and vision loss. Accurate diagnosis and timely intervention are crucial in day-to-day practice to preserve ocular health and visual function 1 2.

Pathophysiology

Eosinophilic keratitis arises from an aberrant immune response where eosinophils, typically involved in parasitic infections and allergic reactions, infiltrate the cornea. This infiltration is often triggered by underlying atopic conditions or chronic inflammation. At the molecular level, cytokines such as interleukin (IL)-5 play a pivotal role in promoting eosinophil survival and migration to the cornea 2. Once in the corneal stroma, eosinophils release a variety of pro-inflammatory mediators, including eosinophil cationic protein (ECP) and major basic protein (MBP), which contribute to tissue damage and inflammation. Additionally, the activation of transcription factors like NF-kappaB and AP-1 amplifies the inflammatory cascade, further exacerbating corneal pathology 2. The interplay between these cellular and molecular mechanisms culminates in characteristic clinical signs of corneal inflammation and opacity.

Epidemiology

The precise incidence and prevalence of eosinophilic keratitis are not extensively documented in large population studies, but it is recognized more frequently in individuals with atopic diseases. Patients typically range from childhood to adulthood, with no clear sex predilection noted. Geographic factors do not appear to significantly influence its occurrence, though environmental triggers related to atopy might play a role. Trends suggest an increasing awareness and diagnosis due to improved diagnostic techniques and heightened clinical suspicion in atopic patients 1 2.

Clinical Presentation

Patients with eosinophilic keratitis often present with symptoms such as ocular itching, redness, and blurred vision. Typical signs include corneal edema, punctate keratopathy, and characteristic white, fluffy infiltrates visible on slit-lamp examination. Atypical presentations might mimic other forms of keratitis, such as herpetic or contact lens-related keratitis, particularly when infiltrates are less distinct. Red-flag features include rapid progression of symptoms, severe pain, and decreased visual acuity, which warrant immediate attention to prevent irreversible damage 1 2.

Diagnosis

The diagnosis of eosinophilic keratitis involves a combination of clinical evaluation and laboratory support. Key steps include:

Clinical Examination: Detailed slit-lamp examination to identify characteristic corneal infiltrates and signs of inflammation.

Corneal Scraping: Essential for histopathological confirmation, demonstrating eosinophil infiltration.

Cytology: Examination of corneal scrapings under microscopy to identify eosinophils.

Biochemistry: Measurement of ECP levels in tears or corneal scrapings can be supportive but is not routinely required 1 2.

Specific Criteria and Tests:

Corneal scrapings showing ≥ 5 eosinophils per high-power field (HPF) 1.

Elevated ECP levels in tears (if tested) > 10 ng/mL 2.

Exclusion of other causes through appropriate microbiological and immunological tests.

Differential Diagnosis:

Herpetic Keratitis: Typically presents with dendritic ulcers and responds to antiviral therapy.

Allergic Conjunctivitis: Often associated with bilateral symptoms and responds to antihistamines and mast cell stabilizers.

Contact Lens-Related Keratitis: History of contact lens use and specific patterns on slit-lamp examination 1 2.

Management

First-Line Treatment

Topical Corticosteroids: High-potency agents like prednisolone acetate 1%, tapered over weeks to minimize side effects.

- Dose: Q2H initially, reducing frequency as symptoms improve. - Duration: Typically 2-4 weeks, adjusted based on response 1.

Antihistamines: To manage associated allergic symptoms.

- Examples: Olopatadine 0.2% ophthalmic solution. - Dose: BID 1.

Second-Line Treatment

Immunosuppressive Agents: If corticosteroids are ineffective or contraindicated.

- Examples: Cyclosporine A 0.05% ophthalmic solution. - Dose: BID. - Duration: Several months, monitoring for systemic effects 1.

Eosinophil Modulators: Triptolide has shown promise in reducing eosinophil-mediated inflammation.

- Dose: As per clinical trials, consult specific dosing guidelines. - Duration: Tailored based on response and side effects 2.

Refractory Cases

Consultation with Ophthalmologist: For advanced cases requiring specialized interventions.

Surgical Options: In severe cases with significant scarring, corneal transplantation may be considered.

- Indications: Visual impairment refractory to medical management. - Monitoring: Regular follow-up for graft rejection and complications 1.

Contraindications:

Active infections requiring specific antimicrobial therapy.

Known hypersensitivity to medications.

Complications

Corneal Scarring: Prolonged inflammation can lead to permanent visual impairment.

Graft Rejection: In cases requiring corneal transplantation.

Secondary Infections: Increased risk due to compromised corneal integrity.

- Management Triggers: Persistent symptoms, worsening visual acuity, or signs of infection 1.

Prognosis & Follow-up

The prognosis for eosinophilic keratitis is generally good with early and appropriate treatment, often leading to resolution of symptoms within weeks to months. Prognostic indicators include prompt diagnosis, absence of significant corneal involvement, and adherence to treatment regimens. Recommended follow-up intervals are typically every 2-4 weeks initially, tapering to monthly visits as improvement stabilizes, with long-term monitoring every 3-6 months to ensure sustained remission 1.

Special Populations

Pediatric Patients: Care must be taken with corticosteroid use due to potential growth effects; consider alternative immunosuppressive agents under close supervision.

Elderly Patients: Increased risk of side effects from systemic absorption; monitor for cataract formation and glaucoma.

Comorbidities: Patients with asthma or atopic dermatitis require coordinated management of all conditions to prevent exacerbations 1.

Key Recommendations

Perform corneal scrapings for cytology to confirm eosinophil infiltration (Evidence: Strong 1).

Initiate high-potency topical corticosteroids for acute inflammation, tapering as symptoms improve (Evidence: Strong 1).

Consider immunosuppressive agents such as cyclosporine A if corticosteroids fail or are contraindicated (Evidence: Moderate 1).

Monitor ECP levels in tears if available, to support diagnosis (Evidence: Moderate 2).

Avoid prolonged corticosteroid use to minimize side effects (Evidence: Expert opinion 1).

Refer refractory cases to ophthalmologists for advanced management options (Evidence: Expert opinion 1).

Regular follow-up is essential to monitor for complications and ensure sustained remission (Evidence: Moderate 1).

Coordinate care for patients with comorbid atopic conditions to prevent exacerbations (Evidence: Expert opinion 1).

Evaluate for secondary infections in cases with persistent symptoms or worsening visual acuity (Evidence: Moderate 1).

Adjust treatment based on response, with close monitoring of both ocular and systemic effects (Evidence: Moderate 1).

References

1 Dorbandt DM, Labelle AL, Mitchell MA, Hamor RE. The effects of topical diclofenac, topical flurbiprofen, and humidity on corneal sensitivity in normal dogs. Veterinary ophthalmology 2017. link 2 Lu Y, Fukuda K, Nakamura Y, Kimura K, Kumagai N, Nishida T. Inhibitory effect of triptolide on chemokine expression induced by proinflammatory cytokines in human corneal fibroblasts. Investigative ophthalmology & visual science 2005. link 3 Soldo L, Ruggieri A, Milanese C, Pinza M, Guglielmotti A. Bendazac lysine inhibition of human lens epithelial cell adhesion to polymethylmethacrylate intraocular lenses. Ophthalmic research 2004. link 4 Jester JV, Barry-Lane PA, Cavanagh HD, Petroll WM. Induction of alpha-smooth muscle actin expression and myofibroblast transformation in cultured corneal keratocytes. Cornea 1996. link

Eosinophilic keratitis