As a substudy of the FDA phase III clinical trial of CK, my colleagues and I examined the incidence and effects of any astigmatism induced by the procedure in 203 patients. Surgically induced astigmatism was one of the FDA's safety variables that we wanted to study more carefully. This group of patients has been analyzed at the 1-year postoperative visit, but the clinical trial now has 2-year follow-up data. In this substudy, we analyzed both absolute and vectoral changes in astigmatism and based on these results, made some recommendations regarding the prevention and care of surgically induced astigmatism that may occur with CK.
ABSOLUTE VERSUS VECTORAL ANALYSIS
By studying the incidence and natural history of absolute changes in refractive cylinder, we found that the incidence of postoperative refractive cylinder for CK patients decreased over time. In the patients we studied, the absolute change in refractive cylinder (>1.0 D) at 1 month postoperatively was 21%, degrading to 15% at 3 months, 14% at 6 months, and 6% at 12 months. I should note that these patients were treated just once with CK and that the clinical trial did not permit retreatments. However, absolute astigmatism is not the most appropriate means by which to evaluate astigmatism. Using a consistent cohort of 203 eyes at the 1-year examination, we performed a vectoral analysis of the astigmatism to identify it more precisely (Figure 1).
When evaluating absolute astigmatism, the surgeon simply looks at the difference in magnitude between refractions pre- and postoperatively. Because surgically induced astigmatism also takes into account the angle of astigmatism, the numbers tend to be higher when evaluating it compared to absolute astigmatism. For instance, a patient who has 1.0 D of astigmatism at 180º preoperatively and no astigmatism postoperatively has an absolute loss of 1.0 D of astigmatism but a vectoral increase of 1.0 D. Similarly, a patient who has 1.0 D at 180º preoperatively and 1.0 D at 90º postoperatively has an absolute change of zero, but his surgically induced astigmatism is actually 2.0 D at 90º. Thus, surgically induced astigmatism by vectoral analysis takes into account the importance of directionality in astigmatism.
When we conducted a vectoral analysis of the CK patients, we found that the centroid of surgically induced astigmatism was 0.23 D of steepening at 175º, which was statistically significant (Figure 2). On average, this slight induction of astigmatism goes against the rule. When we examined the absolute magnitude of the surgically induced astigmatism, which includes both those patients whose astigmatism improved and those whose worsened, we found an average of 0.66 D of surgically induced astigmatism.
We reviewed the literature on a variety of refractive surgery procedures including PRK, LASIK, and the intracorneal ring, and found that the mean surgically induced astigmatism and magnitude for CK were comparable to that of these other procedures. For instance, two studies we conducted of LASIK and PRK, although not strictly comparable, showed a mean of 0.2 D at 86º in LASIK and of 0.5 D at 92º in PRK, with respective magnitudes of 0.88 and 0.99 D. A study of hyperopic PRK showed a mean surgically induced astigmatism of 0.15 D with a magnitude of 0.52 D.
A number of technical recommendations are helpful in preventing induced astigmatism during CK. First, it is important in a thermal keratoplasty procedure to have excellent centration, as decentration could induce astigmatism. My colleagues and I prefer to mark directly over the entrance pupil. At the slit lamp, I mark the patient's horizontal and vertical axes directly over the slit beam, which I place at either 90º or 180º directly through the pupil. I use those limbal positioning marks as a cross, the intersection of which will be directly over the pupil's center, to help align the CK marker. I find this technique helpful in achieving good centration after the procedure. It is important to meticulously place the initial CK applications to keep a perfect centration; the first four marks in particular help center the procedure.
The second recommendation for minimizing the risk of induced astigmatism with CK is to work with a consistently dry corneal surface. Areas of tears, water pooling, or excessive dryness can cause an inconsistent uptake of the radiofrequency energy. Third, the CK treatment must be delivered perpendicular to the cornea. To do so, I rotate my wrist to ensure that the entry angle into the cornea is perpendicular to the area I am entering. After feeling the “pop” as the probe enters through Bowman's, I prefer to allow the cornea to seat around the CK probe before applying thermal energy. I wait 1 or 2 seconds to allow deep penetration before creating the spot. The probe itself is 450 X 90 µm, and the tip should be engaged into the cornea over its full extent. Fourth, between applying each ring of CK treatment, I inspect the tip for any buildup of epithelial cells that could cause inconsistent depth. Finally, a study by Daniel Durrie, MD, (Kansas City, Missouri) suggests that patients who have irregular astigmatism or a noncentered corneal apex revealed on Orbscan topography (Bausch & Lomb Surgical, San Dimas, CA) prior to treatment could be prone to surgically induced astigmatism following CK (personal communication, Daniel Durrie, MD, May 2002). Therefore, you may want to take special care of these patients or avoid treatment altogether.
We are currently exploring the following treatment method options for induced astigmatism following CK. The first uses intraoperative keratometry to apply additional spots in the flat meridian if the cornea is not spherical after the initial treatment. This method has not been tested yet, but we are planning to study it in clinical trials in our center. Another option is a CK en-hancement for surgically induced astigmatism following the initial surgery. We are also formulating a clinical trial for this approach, which would include options such as adding extra treatment spots to the flat axis. In cases of surgically induced astigmatism, we prefer to apply additional spots in the periphery (usually in the 8- or 9-mm optical zone) to help steepen the flat axis. We are currently working on developing our own nomograms (including the number of spots and zone diameters) for these options. Initial results are encouraging.
We followed the study patients for 2 years and made two important findings. First, most surgically induced astigmatism tends to degrade by itself over time, so surgeons should not be too quick to perform enhancements. I believe that over time, both the axis and magnitude of astigmatism change, and normal healing generally ameliorates the astigmatism. Second, if considering performing an enhancement, be conservative. The beauty of CK is that it is a relatively simple and safe procedure, so adding spots on another day is easy for both surgeon and patient.
In general, I believe the best CK patient is older and moderately hyperopic (although ongoing studies using CK for plano presbyopes are very encouraging). In many cases, patients who are spherical and without astigmatism preoperatively, patients whose topography shows a well-centered corneal apex, and those who have no irregular astigmatism or only slight topographic astigmatism will likely fare the best.
There tends to be particular concern about surgically induced astigmatism in hyperopia procedures. As we have shown, this occurrence, while present in some patients in the early postoperative period, tends to diminish over time. Surgeons will be able to minimize this risk using proper technique. Paying such attention to detail makes CK a safe and patient-friendly modality for treating hyperopia.