Article

TREATMENT PLAN

THE EFFECTS OF DIABETES ON THE OCULAR SURFACE

The systemic health effects of diabetes are well known and affect multiple organ systems. Most familiar to eye-care practitioners are the effects of diabetes on the retina and crystalline lens. Often forgotten are the effects of diabetic hyperglycemia on the cornea and ocular surface. Specific to this are conditions observed in clinical practice that can include diabetic keratopathy and dry eye disease. It has been estimated that one- to two-thirds of all diabetic patients have some form of diabetic keratopathy, many of which are undiagnosed (Schultz et al, 1981; Rao et al, 1987; Kaji, 2005; Wylegala et al, 2006). A higher risk for either keratopathy or dry eye occurs in patients who have higher hemoglobin A1c levels and longer duration of diabetes.

While the posterior segment of diabetic patients is carefully monitored during eye examinations, the ocular surface and cornea should also be regularly assessed, especially in patients who have proliferative diabetic retinopathy (Gao et al, 2015).

Managing Diabetes-Induced Dry Eye

Although different in causation, the clinical effect of diabetes-induced dry eye disease is similar, and thus treatment is not unlike that of other dry eye conditions. The pathogenesis of diabetic dry eye consists of interrupting the feedback loop for tear secretion as a result of aberrant ocular surface sensitivity. This may lead to decreased tear breakup time, increased tear osmolarity, and ocular surface inflammation. There may also be a decreased blink rate and decreased tear supplement use in this patient population (Inoue et al, 2004; Nepp et al, 2000).

Your treatment would include topical tear supplements and punctal occlusion in cases of moderate dry eye disease. More severe forms may require topical steroids, non-steroidal anti-inflammatories, and cyclosporine ophthalmic emulsion. However, the long-term use of steroids may predispose the eye to ocular infection, elevated intraocular pressure, and cataracts. In cases of severe dry eye disease, another more recent treatment may include lifitegrast. In addition to managing the overall ocular surface, you will also need to likely treat the cornea.

Diabetic keratopathy can be staged using a scale developed by Mackie (1995), which progresses from mild ocular surface changes to stromal involvement. Diabetic keratopathy will appear as corneal erosions that are persistent and prone to recur. The erosions can be quite resistant to conventional treatments. The result is corneal edema and, over time, corneal scarring. The corneal edema can be treated with 2% or 5% sodium chloride solution or ointment.

As in dry eye, the loss of corneal sensation causes a disruption in homeostasis that weakens the adhesion between the epithelial basement membrane and the underlying stroma. Anterior stromal puncture with a 25-gauge needle, or phototherapeutic keratectomy, can be performed in cases of recurrent corneal erosions.

Adding to the corneal insult is the delay in healing in diabetic patients. In rare cases, this may lead to stromal ulceration or perforation. In addition to the superficial damage that may occur to the cornea, the endothelium may also exhibit polymegethism/polymorphism and edematous changes that may include the stroma. Treatment can include tear supplements in mild cases. Severe and recalcitrant cases may benefit from bandage contact lenses or amniotic membranes to protect the corneal surface, prevent ulceration, and aid in re-epithelialization. Amniotic membranes also provide beneficial growth factors for efficient healing. Topical application of antibiotics may also be warranted as a prophylaxis against microbial keratitis in an at-risk cornea.

Current work has also investigated adenoviral gene and stem cell therapies to treat diabetic keratopathy (Kramerov et al, 2016; Kramerov and Ljubimov, 2016). Other investigative topical drops include those containing substance P, insulin-like growth factor-1, nerve growth factor, and opioid growth factor (Yamada et al, 2008; Bonini et al, 2000; Zagon et al, 2006). CLS

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