The cornea is a unique transparent avascular tissue and the main ocular structure responsible for light refraction. Any alteration to its surface regularity and optical transparency can interfere with light refraction, causing reduced visual acuity, increased optical aberrations, distorted images, and loss of contrast sensitivity.
Ocular surface disease potentially can affect a patient’s quality of life, and it also can be a contraindication for refractive surgery. Therefore, extensive preoperative examination is mandatory. This article provides our top tips for evaluating the cornea and ocular surface, emphasizing three areas: epithelial defects, stromal opacities, and endothelial dysfunction.
Evaluation of the ocular surface should take into account surface lubrication, as measured by tear breakup time and Schirmer test. Additionally, the optical quality of the corneal surface should be evaluated by examining the regularity of the optical rings of a Placido disc reflected by the corneal surface. In eyes with epithelial defects and unevenness or a high viscosity of tears, the keratoscopy rings appear irregular, with broken and uneven edges. A poor interface between the corneal surface and air, due to lack of tears or epithelial defects, causes poor image quality transfer from the cornea to the retina.
In eyes with good tear lubrication, on the other hand, the presence of epithelial defects inferiorly combined with superficial fine neovascularization could be related to any one of several factors that must be investigated to avoid recurrence and guarantee proper treatment. Complete turnover of the epithelium takes roughly 7 days and is sustained by epithelial stem cells present at the limbus; if part of the basement membrane is stripped, the surrounding cells rapidly slide and migrate to fill the defect. When this process is impaired, night exposure of the eye due to Bell phenomenon may be suspected. Skin rosacea and vernal conjunctivitis, both of which are common in atopic children and adults, may also be suspected.
Epithelial defects associated with corneal neovascularization, stromal thinning, and induced irregular astigmatism can be misinterpreted as corneal conjunctivalization due to limbal stem cell deficiency. Although this rare condition is misdiagnosed and overestimated, it can be associated with chronic inflammation, neovascularization, scarring, ulceration, melting most frequently caused by chemical and thermal injuries, and inflammatory conditions as Stevens-Johnson syndrome. In rare cases, it can also be related to genetic defects causing aniridia and congenital cataract. Chronic contact lens epitheliopathy or contact lens solutions can induce mild trauma to limbal stem cells.
Mild punctal erosions, recurrent erosions, and delay of reepithelialization after minor trauma could be due to Bowman membrane dystrophies and congenital or acquired corneal hypoesthesia, which are often associated with surgical or traumatic damage to the trigeminal nerve, tumors (neurofibroma or angioma), or infections (herpes zoster ophthalmicus or herpes simplex keratitis). Trigeminal nerve dysfunction results in decreased lacrimal and conjunctival tear secretion and poor epithelial adhesions. Once an epithelial defect develops, infection or stromal ulceration often follows. Hypoesthesia and the presence of feeding vessels are usual signs and symptoms associated with corneal opacities and leucomas related to herpes simplex infections.
In the presence of epithelial defects, sources of ongoing inflammation must be eliminated with antiinfective or immunomodulatory therapy, such as topical diaminodiphenyl sulfone in cases of ocular cicatricial pemphigoid. Infectious causes of inflammation should be treated with antiinfectives, but the use of potentially toxic topical medications should be minimized.
To address ocular surface dryness, treatments include preservative-free lubricating agents and, depending on the severity, punctal occlusion. Meibomian gland dysfunction should be treated with warm compresses, lid hygiene, and doxycycline. Excessive eye exposure, chronic reepithelialization delay, and neurotrophic ulcers can be addressed with soft bandage contact lenses and ointment, temporary tarsorrhaphy with botulin toxin injection, or permanent mediolateral surgical tarsorrhaphy.
Encompassing about 90% of the cornea’s thickness, the stroma consists of flattened lamellae composed of collagen fibrils embedded in a matrix of proteoglycans. The highly regular architecture of the stroma is a major determinant of corneal transparency. Corneal scarring modifies the regular architecture of stromal fibrils and reduces transparency. Stromal opacities that occur as a result of corneal trauma or infection can be a source of visual impairment.
Thorough preoperative evaluation to determine the depth, proximity to the visual axis, and visual significance of any corneal opacity is essential in surgical planning and optimization of visual outcomes. The depth of the opacity can be estimated at a slit lamp with a narrow slit, and anterior segment optical coherence tomography (OCT) can provide precise and reproducible localization and quantification of the depth and extension of stromal opacities, whatever their density or hyperreflectivity. Because the OCT light source goes through these opacities, thickness and relative positioning can be assessed without scattering or deviation of light waves. Depending on the opacity and its localization and depth, different surgical techniques may be considered to eliminate the pathology and restore corneal smoothness. Choices include phototherapeutic keratectomy and superficial or deep anterior lamellar keratoplasty.
ENDOTHELIAL DYS FUNCTION
The Descemet membrane is secreted by endothelial cells starting at fetal age, but the membrane’s cells do not regenerate. This basement membrane has an elastic quality, and, once split, it retracts and rolls on itself. The corneal endothelial cells play a major role in preserving stromal transparency; they regulate corneal hydration through barrier and pump functions.
Assessment of the corneal endothelium and its function should include quantification and shape evaluation of endothelial cells in the central and peripheral cornea with biomicroscopy, in addition to corneal thickness measurements taken throughout the day. A 10% to 30% variation in central corneal thickness between morning and evening indicates poor regulation of corneal hydration due to a low number and poor functioning of endothelial cells. However, this condition can be well tolerated by a patient if there is good visual acuity and minimal reduction of stromal transparency. These cases require only observation until surgery is indicated.
When cataract is associated with endothelial dysfunction, such as in Fuchs dystrophy, peripheral assessment of the endothelial pool and the morphologic characteristics of the cells is mandatory. Phacoemulsification and IOL implantation alone should be attempted only if the prognosis for corneal transparency is good and the peripheral cell count is at least 1,800 cell/mm2 (Figures 1 and 2). Otherwise, a triple procedure should be planned, with phacoemulsification and IOL implantation performed just before endothelial transplantation.
Ocular surface evaluation should always include thorough assessment of the corneal surface for optical quality and tear lubrication. Whether the cornea is affected by epithelial defects, stromal opacities, or endothelial dysfunction, any corneal condition must be treated prior to surgery to avoid reduced visual acuity, aberrations, distorted images, and contrast sensitivity loss postoperatively.
Elena Albè, MD, is a Consultant in the Department of Ophthalmology, Cornea Service, Istituto Clinico Humanitas Ophthalmology Clinic, Milan, Italy. Dr. Albè is a member of the CRST Europe Editorial Board. She states that she has no financial interest in the products or companies mentioned. She may be reached at e-mail: email@example.com.
Massimo Busin, MD, is Head of the Department of Ophthalmology at Villa Serena Hospital, Forli, Italy. Dr. Busin states that he has a royalty agreement with Moria SA. He may be reached at e-mail: firstname.lastname@example.org.