Effects of contact lens-induced hypoxia on the physiology of the corneal endothelium. Optom Vis Sci ; Quinn TG. Epithelial folds.
Handling Contact Lens Complications
Corneal edema with polymethylmethacrylate versus gas-permeable rigid polymer contact lenses of identical design. J Am Optom Assoc ; Rengstorff RH. Corneal curvature and astigmatic changes subsequent to contact lens wear. Woods CA, Efron N. Regular replacement of extended wear rigid gas permeable contact lenses. CLAO J ; Ocular effects of hard gas-permeable-lens extended wear. Am J Optom Physiol Opt ; Norn MS. Fluorescein vital staining of the cornea and conjunctiva. Acta Ophthalmol Copenh ; Allansmith MR.
Pathology and treatment of giant papillary conjunctivitis. This is another relatively common condition associated with soft contact lens wear. Hypoxia from a tight-fitting lens is one of the primary reasons new vessels invade the unvascularized cornea. In some cases, the cause is an old immune infiltrate, which may have lingering vessels even after the original infiltrate is gone. Sensitivity to a cleaning solution may also trigger superior corneal neovascularization. In some cases, excessive lens deposits have caused or contributed to the hypoxic condition, perhaps by altering the Dk value of the lens.
Deep stromal vessel growth, though rare, is of greater concern and, if left unchecked, can lead to significant complications. When you're faced with this type of corneal neovascularization, keep in mind the differential diagnosis of interstitial keratitis, including syphilis. Most peripheral neovascularization micropannus is considered clinically insignificant, however if vessels intrude beyond about 1.
Patients in an extended wear lens schedule should be moved to a daily wear schedule. Reconsider the lens fit as well as the oxygen transmissibility value. Up to a point, the Dk may be a factor in ensuring the cornea is not deprived of oxygen. As with all ocular abnormalities, monitor neovascularization closely.
Vessel growth into the visual axis, although exceptionally rare, can lead to visual impairment via intracorneal hemorrhage, lipid exudation and scaring, all of which potentially compromise the patient's vision. GPC is a hypertrophy of the upper tarsal conjunctiva induced by chronic ocular trauma of the lid against ocular prostheses, nylon sutures, exposed scleral buckles and, most commonly, contact lenses. A mechanical mechanism of roughly 6, blinks a day combined with an inflammatory response is believed to be the cause of GPC.
The papillae will be nestled in thickened and hyperemic conjunctival tissue with hyperplastic epithelium growing into the stromal layer. Mucous production, contact lens intolerance, ocular irritation, itching, injection, foreign body sensation and excessive lens movement are all symptomatic of GPC and help confirm the diagnosis. Treatment of moderate to severe contact-lens induced GPC is rather intuitive: Remove the causative factor or reduce use of the contact lenses. Also consider exchanging the lens for one with a different edge and polymer modulus.
This may help combat the mechanical aspects of GPC. Symptoms usually subside quickly after these adjustments, but it will take longer for the papillae to return to normal.
One study has shown that the incidence of GPC is decreased in subjects who wore lenses for three weeks or less. Herpes simplex virus-1 keratitis is the most frequently seen viral condition.
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Though not usually associated with contact lens wear, HSV keratitis may appear with little warning and, often, apparently no provocation. The HSV-1 lies dormant in roughly 90 percent of the adult population after initial infection via mucocutaneous distribution to the trigeminal nerve. The virus spreads from the infected epithelial cells to the sensory cells, down the nerve axon and eventually to the trigeminal ganglion, where it enters the neuron nucleus and lies dormant. However, even after decades of dormancy, factors such as emotional or physical stress, overexposure to UV light, hormonal changes and certain medications such as prednisone can trigger the emergence of HSV keratitis.
The patient will report redness, tearing, photophobia and blurry vision, but a definitive diagnosis comes from close examination of the corneal vesicles and dendritic ulcers. Though contact lens-related pseudo-dendrites and large corneal abrasion healing patterns can confuse the diagnosis, 6 HSV antigen detection tests and viral cultures confirm it. Antiviral therapy will speed resolution of the keratitis and limit stromal damage and scarring.
Begin aggressive treatment with trifluridine or vidarabine, and oral acyclovir, accompanied by close observation. Bacterial keratitis is arguably the most serious complication of contact lens wear.
Fortunately the eye has non-specific defense mechanisms to deter infection. The lids wipe and cleanse the ocular surface; tears flush out debris and pathogens; there is continual sloughing of old epithelial cells being replaced with new healthy cells as well as the immune response system in the tear film, limbus and epithelium.
However, despite the eye's defenses, daily lens wearers and, more frequently, extended-wear lens patients present with microbial keratitis every year. Pseudomonas aeruginosa , Staphylococcus aureus and Staphylococcus epidermidis have slightly different modes of attack but are the most commonly cultured bacteria.
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