Mechanism corneal damage in allergic conjunctivitis

During the ocular inflammatory process the tear film undergoes a significant change, contributing to a wide range of corneal clinical manifestations.

Inflammatory cells are seen in the tear film.
Cytokines and chemokines liberated from mast cells, eosinophils, and Th1 and Th2 cells, can be identified in the tear film of ACK and VKC patients.
An upregulation of cytokine production by stromal keratocytes has been documented after stimulation with cytokines typical of the allergic reaction such as IL-4 and TNF-α.
It is worth noting that corneal pathology in allergic eye disease appears to be related to the degree of inflammation rather than the mechanical size of giant papillae.
There is also demonstrable mechanical tear film instability, owing in part to changes in the mucin layer of the tear film, changes in corneal sensitivity and possible changes in the corneal epithelium permeability.

All of these may act together in the pathogenesis of punctate keratopathy and eventually confluent ulceration and shield ulcer.

In addition, there is increased mechanical eye rubbing and changes in corneal stromal keratocytes that contribute to the development of keratoconus. Patients with systemic atopy have immunosuppression, contributing to an increased risk of infectious keratitis.

There is increasing evidence of involvement of lymphocytes of the Th17 subclass in some allergic diseases, but at the moment their role in allergic eye disease is yet to be fully elucidated.

Grading shield ulcer:
Grade 1 = shield ulcer with a clear base; these have a favorable outcome and re-epithelization with mild scarring;
Grade 2 = ulcers with visible inflammatory debris at the base; such ulcers are prone to complications and exhibit delayed re-epithelization and a poor response to medical therapy;
Grade 3 = shield ulcers with elevated plaques (Figure 4). These respond best to surgical therapy.

The longer the shield ulcer persists, the greater the likelihood of sterile ulceration, corneal scars, bacterial keratitis, amblyopia and globe perforation.

Limbal and peripheral cornea involvement is characterized by multiple gelatinous, yellow-gray limbal infiltrates. The size and the location of these infiltrates may change over time. The limbus may appear thickened and opacified for 360°, accompanied by a peripheral, superficial neovascularization. The apices of these infiltrates may appear as punctate calcified concretions called Tranta's dots. Papillae formation of the limbus may develop in severe cases as a result of fibrovascular growth.

Superficial and stromal vessels may develop in response to persistent ulcer and plaques growing from the limbus reaching the plaque. The VEGF family of cytokines and their receptors are involved in both angiogenesis and microvascular permeability. An imbalance between angiogenic and antiangiogenic factors may contribute to severe corneal neovascularization that can develop in severe AKC and VKC.

The chronic inflammation seen in severe limbal VKC and AKC patients may lead to gradual loss of corneal limbal stem cell function. This may occur due to impaired mechanical stromal support or direct damage to the stem cells by the toxic products of eosinophils and other inflammatory cells infiltrating the limbus. Partial or total limbal stem cell deficiency (LSCD) can be one of the complications of long-standing VKC, contributing to severe visual impairment in young individuals.

Pseudogerontoxon, which resembles arcus senilis, is a waxing and waning grey-white lipid deposition in the superficial stroma of the peripheral cornea. It is an uncommon complication of VKC, and, although it does not affect visual function, it may persist for years, even in the absence of limbal inflammation.

In the management of VKC and AKC, patients and parents should be informed of the cause and duration of the disease, and its possible complications. Avoidance of nonspecific triggering factors such as sun, wind and salt water, with the use of sunglasses, hats with visors and swimming goggles, respectively, must be recommended. Frequent hand and face washing should be also suggested.

Drug tx:
Mast cell stabilizer
Topical antihistamines
Topical NSAID
The best for mod-severe case: steroid
-1st choice low systemic absorption: fluorometholone, clobetasone
-2nd pred/dexa/beta

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