Introduction
The central toxic keratopathy (CTK) syndrome is an uncommon, acute, non-inflammatory condition that, following refractive surgery, causes widespread opacification of the center corneal stroma. Fortunately, central toxic keratopathy and other problems following refractive surgery are uncommon, although refractive procedures are generally recognized and often carried out worldwide.
In addition to the normal central corneal opacification that appears 3–9 days following refractive surgery, stromal tissue loss and a sizable hyperopic refractive shift are common symptoms of central toxic keratopathy. Despite the fact that striae often characterize central toxic keratopathy, the illness can also exist without them. Usually, it takes 2 to 18 months for the central toxic keratopathy results to disappear.
What Are the Causes of Central Toxic Keratopathy?
Several speculations about what could have caused central toxic keratopathy, despite its specific etiology, are unknown.
The most well-known hypotheses in the literature include the following:
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Excimer laser's photoactivation of povidone-iodine.
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Laser-induced keratocyte apoptosis of the corneal matrix.
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Intraoperative exposure to meibomian gland secretions.
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Talc from latex surgical gloves.
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Post-operative debris from the microkeratome blade.
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The microkeratome blade leaves behind surgical waste.
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Additionally proposed as potential causes of center toxic keratopathy are the length of laser exposure and the kind of laser utilized in refractive operations.
What Is the Pathophysiology Associated With Central Toxic Keratopathy?
Some parts of the illness have been established, but the pathophysiologic alterations in central toxic keratopathy are not fully understood. Thinning of the cornea due to stromal loss is one of the disease's main features. Apoptosis of keratinocytes is the hypothesis with the greatest evidence to explain the underlying process. The observed central opacity can potentially result from this mass keratinocyte death. Anterior tangential curvature is lost due to tissue loss, which is most noticeable in the first month. However, posterior tangential curvature is mostly unaffected. A counterargument to the observed thinning claims that modest stretching is brought on by microadenoma in the corneal periphery.
What Are the Signs and Symptoms Associated With Central Toxic Keratopathy?
The following are the symptoms associated with central toxic keratopathy:
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Photophobia (It is a condition in which bright lights might harm the eyes).
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Discomfort.
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Floaters (Small fragments of the protein collagen make up floaters).
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Redness.
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Halos (Bright circles around a light source, such as headlights, are known as halos).
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A shift towards hyperopia (It is a condition of the eyes whereby distant things are often regarded as being clearer than those that are close).
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CTK often results in decreased best spectacle-corrected visual acuity (BSCVA).
The most common sign of central toxic keratopathy are:
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Striae, stromal tissue loss.
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Thick central corneal opacification.
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A sizable hyperopic refractive shift.
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The central corneal opacification in central toxic keratopathy may start as diffuse lamellar keratitis (DLK) on postoperative day 1 or 2, swiftly progressing to a dense opacification of the central corneal stroma.
How to Manage Central Toxic Keratopathy?
Close monitoring and routine follow-up appointments continue to be the most significant care approach for patients with central toxic keratopathy because the centralized stromal haze in central toxic keratopathy spontaneously disappears after 18 months without therapy. Although corticosteroids were once used to treat central toxic keratopathy, their use has been discouraged in light of current research showing that the condition is not inflammatory and is not sensitive to steroid therapy.
Additional medicinal treatments that may be helpful include metalloprotease inhibitors like Doxycycline and substances that hasten corneal wound healing (like Ascorbic acid); however, substances like Mitomycin-c, which are known to disrupt these processes, may worsen results in people with central toxic keratopathy. Last but not least, some have used hyperosmotic drugs.
Surgery is debatable because of concern for additional corneal thinning and the disease's major hallmark of stromal tissue loss. However, using more intrusive treatments (such as flap lift and irrigation) to treat central toxic keratopathy shows that extra stromal loss is not unavoidable. According to one study, individuals who had surgical care exhibited less corneal flattening and thinning and had better visual acuity than patients who did not.
Usually, center toxic keratopathy spontaneously recovers after 18 months with few problems or long-term effects. Most issues that develop in the context of center toxic keratopathy, however, usually originate from improper use of steroids or other comparable drugs and can worsen whatever anatomical or refractive changes the patient already has. There may be a decent to favorable prognosis for center toxic keratopathy. Within 18 months of the triggering event, the disease usually clears up. However, hyperopic vision abnormalities may linger.
Conclusion
After LASIK and other refractive surgeries, a self-limited, non-inflammatory condition known as central toxic keratopathy develops. Because central toxic keratopathy and other illnesses have similar clinical characteristics, they are frequently confused for more severe inflammatory and infectious disease processes. The optimal care of central toxic keratopathy differs from the inflammatory and viral illnesses it resembles because of its non-inflammatory nature. Therefore, clearly distinguishing between central toxic keratopathy and various other diseases is still essential to providing the best possible results for people with central toxic keratopathy. If identified appropriately, the prognosis for central toxic keratopathy may range from fair to good. Most of the time, the ailment becomes better within 18 months after the trigger.
