Recession of a single rectus muscle typically causes a decrease in corneal curvature in the meridian of the recessed muscle, although it can occasionally paradoxically increase the focusing power along this meridian.1–6 This effect is most likely related to a change in corneal curvature secondary to the reduction in tension of the recessed extraocular muscle transmitted via the sclera to the cornea.7–9 There may be some difference in the degree of extraocular muscle tension to the cornea according to the amount of a single rectus muscle recession. However, there is relatively little information in the literature regarding the consequent changes in astigmatism after strabismus surgery in relation to the amount of recession.10
A clarification of whether the magnitude of induced astigmatism has any correlation to the amount of lateral rectus recession has important implications on the establishment of postoperative management in children with intermittent exotropia. For example, large recession of a single lateral rectus muscle has generally been performed as an alternative to bilateral surgery for moderate angle intermittent exotropia.11–13 Operating on one muscle has the advantages of requiring less time, less anesthesia and placing only one muscle at risk for any possible surgical complications.14 However, if a very large recession induces astigmatism only in the operated eye, then this refractive change might place that eye at risk for amblyopia and nullify some of the advantages of monocular surgery.
This study evaluated the effects of lateral rectus recession on the induced astigmatism in patients who had undergone unilateral or bilateral recession for intermittent exotropia. Statistical analysis was used to determine whether there was any correlation between the amount of lateral rectus recession and the cylinder power (diopter) of the induced astigmatism.
A retrospective analysis was made of 430 patients who had undergone unilateral or bilateral lateral rectus recession for intermittent exotropia between March 2003 and April 2007. Exclusion criteria for this study included children aged 3 years and younger (34 patients), children aged 10 years and older (121 patients), presence of amblyopia (at least a two line difference in Snellen acuity; 33 patients), preexisting ocular abnormalities (16 patients), previous history of ocular surgery (67 patients), coexisting vertical strabismus (59 patients), and follow-up duration <3 months (38 patients).
Sixty-two patients were included in this study. Based on the amount of lateral rectus recession, the patients were divided into two groups: group 1 (34 eyes, 34 patients) with unilateral large recession that was ≥9.5 mm and group 2 (56 eyes, 28 patients) with a bilateral moderate recession that was ≤8 mm. The following parameters were reviewed and analyzed: age, gender, distant and near manifest deviations, amount of lateral rectus recession (mm), preoperative and postoperative noncycloplegic autorefraction and best-corrected visual acuity, and calculated cylinder power and axis of induced astigmatism.
All patients in this study had a complete ophthalmologic examination by the authors. Deviation angles were measured using the alternate prism cover test or by the Krimsky test at each visit. Visual acuities were measured using Snellen's chart or the “E” chart at each visit. Surgery was performed by one of the authors. Under general anesthesia, the surgeon made a limbal conjunctival incision and exposed and recessed the lateral rectus muscle(s) with crossed-swords technique according to patients' deviation angles. The surgeon performed a unilateral large lateral rectus recession (9.5 to 10.0 mm) for the patients with a deviation angle that was ≤25 Δ and a bilateral recession, according to Parks' number, for the patients with a deviation angle that was >25 Δ. Noncycloplegic autorefractions of all the patients were measured at 1 to 3 weeks before surgery and at 1 week, 1 month, and 3 months after surgery. All refractions were obtained with an automated refractometer (KR-8100; Topcon, Tokyo, Japan) by the masked technician. Three consecutive refraction readings were used to arrive at an average refraction result for each patient at each visit.
Induced astigmatism was defined as the difference between each postoperative refraction and the respective preoperative refraction.15,16 Induced astigmatism was calculated by using the double-angle vector analysis, which was first described by Naylor and further developed by Holladay et al., Retzlaff et al., and others.15–18 For the statistical analysis of induced astigmatism, conversion of each data point into an x-y coordinated system was performed according to the methods further described by Holladay et al.17
Example of Subtracting Cylinders Using the Double-Angle Mathematical Methods for Subtraction of Refraction
Step 1: Find x and y components of the vectors representing cylinders
Step 2: Determine the axis of spherocylinder 2 (axis 2)
Step 3: Determine the power of spherocyliner 2 (cylpwr 2)
X = mean value of x, Y = mean value of y
Cylinder power of induced astigmatism = √(X2+Y2), Angle of induced astigmatism = Arctan (Y/X)/2
The cylinder power (D) and the axis (°) of the induced astigmatism were calculated at postoperative time points of 1 week, 1 month, and 3 months. We compared postoperative astigmatism with the corresponding preoperative value with a paired t-test in groups 1 and 2, respectively. In addition, the data for group 1 were compared with those of group 2 with a Student's t-test. To investigate the possible correlation between the amount of lateral rectus recession and the cylinder power of individual induced astigmatism, Pearson correlation coefficient r was calculated.
Statistical analyses were performed with Microsoft Excel (Microsoft Corporation, Redmond, WA) and SPSS version 14.0 (SPSS, Inc., Chicago, IL) software. In all the tests, the level of statistical significance was set at 5% (p < 0.05).
Table 1 summarizes the descriptive data for 62 patients in this study. The average amount of lateral rectus recession was 9.7 ± 0.2 mm (range, 9.5 to 10.0 mm) in group 1 (unilateral large lateral rectus recession) and 7.9 ± 0.3 mm (range, 7.0 to 8.0 mm) in group 2 (bilateral moderate lateral rectus recession). The average cylinder power of preoperative astigmatism was 0.8 ± 1.0 D in group 1 and 0.7 ± 0.8 D in group 2, and there was no difference in cylinder power and axis of preoperative astigmatism between the two groups (p = 0.42).
Table 2 represents the changes in the induced astigmatism over time. At the 1-week follow-up, the average cylinder power of induced astigmatism was 0.8 ± 0.9 D and the axis of induced astigmatism was 91° in group 1, and 0.3 ± 0.5 D and 88° in group 2, respectively. The cylinder power of induced astigmatism for group 1 increased by a larger amount in the with-the-rule direction, i.e., the vertical meridian was more steep than it was for group 2 at the 1-week follow-up (p < 0.01). However, there was no statistically significant difference in magnitude of induced astigmatism between the two groups after the 1-month follow-up. Relaxation of astigmatism was observed towards the preoperative value over time in both groups, however, there was a statistically significant difference in the cylinder power of induced astigmatism compared with that of preoperative astigmatism in both groups until the 3-month follow-up (p < 0.01).
A decreasing tendency in the individual cylinder power of the induced astigmatism over time is illustrated in Fig. 1. At the 3-month follow-up, the frequency of induced cylinder power over 1 D decreased from 24 (8 eyes) to 3% (1 eye) in group 1 and 9 (5 eyes) to 5% (3 eyes) in group 2.
Fig. 2 illustrates the relationship between the amount of lateral rectus recession and the cylinder power of individual induced astigmatism at 1 week after surgery. There was a statistically significant correlation between the amount of lateral rectus recession and the amount of induced astigmatism (Pearson correlation coefficient r = 0.27, p < 0.01).
In this study, changes in astigmatism (induced astigmatism) after lateral rectus recession were evaluated in patients with intermittent exotropia who had undergone unilateral or bilateral recession. In our analysis, there was a statistically significant change in the induced astigmatism in the with-the-rule direction compared with the preoperative astigmatism in both groups until the 3-month follow-up (p < 0.01).
Results of this study correspond with the earlier studies that have reported that recession of a horizontal muscle causes corneal flattening in the meridian of the recessed muscle.2–6,16 Nardi et al.2 reported that the astigmatic changes associated with strabismus surgery were primarily caused by corneal changes rather than changes in the shape of the lens. We postulate that the corneal change after lateral rectus recession is primarily because of the reduction in tension of the recessed muscle. The recession of lateral rectus muscle causes corneal flattening in the quadrant of the recessed muscle, that is, corneal flattening in the with-the-rule direction.1,2 In addition, these results are in close agreement with those of several other authors.3,5,10,16
The most important finding of this study is that our results rejected the hypothesis that there was no correlation between the amount of lateral rectus recession and the amount of cylinder power of induced astigmatism at 1 week after surgery (r = 0.27, p < 0.01). Our results are different from those of Snir et al.19 who reported that there was no correlation between the amount of strabismus surgery and the amount of induced cylinder. Denis et al.10 reported an inverse relationship between the amount of recession and the amount of induced cylinder.
About one-half of the subjects in the Snir et al.'s19 study were <24 months old, and they were comparatively younger than the subjects of our study (mean age, 8 years). Considering that the eye reaches ∼90% of its adult size by age 2 years,20 the astigmatism changes in the Snir et al.'s19 study are not likely to be solely achieved by strabismus surgery. In the Denis et al.10 study, 69 of the 115 patients had undergone inferior oblique recession or medial rectus tucking in addition to medial rectus recession. Because of these simultaneously performed procedures, the inverse relationship may not apply to the all the patients of the Denis et al.'s10 study. However, it is difficult to make a direct comparison between our study and the earlier studies, which did not use vector-based methods to calculate the induced astigmatism.
Larger changes in induced astigmatism were found in group 1 than in group 2 at 1 week after recession (0.8 D, axis 91° vs. 0.3 D, axis 88°, p < 0.01). The difference in magnitude of induced astigmatism at 1-week follow-up was interesting, particularly because the average difference in lateral rectus recession between the two groups is <2 mm. However, this significant difference was not maintained thereafter. Relaxation of astigmatism was observed toward the preoperative value over time in both groups. In addition, there was a relatively more rapid decrease in the cylinder power in group 1 (large recession) than group 2 (moderate recession) from postoperative week 1 to postoperative month 3 (Fig. 1). We find this unexpected difference of the decreasing rates of induced cylinder power interesting; however, the reason for this difference is unknown. Perhaps, this rapid decrease in induced astigmatism in the larger recession group (group 1) has a common mechanism with the more frequent regression toward exotropia observed after larger recessions. Clark and Demer21 explained this by the fact that orbital mechanics can quickly restore the lateral rectus tension after a large recession.
This study has some important limitations that mostly stem from its retrospective design and relatively small range of the amount of lateral rectus recession that was performed. Particularly, there was a gap between 8 and 9.5 mm of lateral rectus recession; however, the authors did not intentionally exclude the patients with these surgical numbers. In addition, the correlation between the amount of recession and the amount of the cylinder power of induced astigmatism might be overemphasized by the two patients with large values (≥3 D) despite of the statistical significance.
In conclusion, large recession of the lateral rectus muscle had more induced astigmatism in the with-the-rule direction than moderate recession during the first week after surgery. However, there was no statistically significant difference in the magnitude of induced astigmatism thereafter between the two groups. The results obtained here suggest that large lateral rectus recession does not seem to produce a sustained astigmatic change compared with moderate lateral rectus recession.
This paper was presented in part as a poster at the 34th Annual Meeting of the American Association for Pediatric Ophthalmology and Strabismus, Washington DC, April 2008.
Department of Ophthalmology
Kyungpook National University
School of Medicine
50 Samduk-2 ga, Jung-gu
Daegu 700-721, South Korea
1.Kwitko S, Feldon S, McDonnell PJ. Corneal topographic changes following strabismus surgery in Grave's disease. Cornea 1992;11:36–40.
2.Nardi M, Rizzo S, Pellegrini G, Lepri A. Effects of strabismus surgery on corneal topography. J Pediatr Ophthalmol Strabismus 1997;34:244–6.
3.Killer HE, Bahler A. Significant immediate and long-term reduction of astigmatism after lateral rectus recession in divergent Duane's syndrome. Ophthalmologica 1999;213:209–10.
4.Reynolds RD, Nelson LB, Greenwald M. Large refractive change after strabismus surgery. Am J Ophthalmol 1991;111:371–2.
5.Kwito S, Sawusch MR, McDonnell PJ, Gritz DC, Moreira H, Evensen D. Effect of extraocular muscle surgery on corneal topography. Arch Ophthalmol 1991;109:873–8.
6.Rajavi Z, Mohammad Rabei H, Ramezani A, Heidari A, Daneshvar F. Refractive effect of the horizontal rectus muscle recession. Int Ophthalmol 2008;28:83–8.
7.Thompson WE, Reinecke RD. The changes in refractive status following routine strabismus surgery. J Pediatr Ophthalmol Strabismus 1980;17:372–4.
8.Preslan MW, Cioffi G, Min YI. Refractive error changes following strabismus surgery. J Pediatr Ophthalmol Strabismus 1992;29:300–4.
9.Hainsworth DP, Bierly JR, Schmeisser ET, Baker RS. Corneal topographic changes after extraocular muscle surgery. J AAPOS 1999;3:80–6.
10.Denis D, Bardot J, Volot F, Saracco JB, Maumenee IH. Effects of strabismus surgery on refraction in children. Ophthalmologica 1995;209:136–40.
11.Nelson LB, Bacal DA, Burke MJ. An alternative approach to the surgical management of exotropia—the unilateral lateral rectus recession. J Pediatr Ophthalmol Strabismus 1992;29:357–60.
12.Dadeya S, Kamlesh. Long-term results of unilateral lateral rectus recession in intermittent exotropia. J Pediatr Ophthalmol Strabismus 2003;40:283–7.
13.Feretis D, Mela E, Vasilopoulos G. Excessive single lateral rectus muscle recession in the treatment of intermittent exotropia. J Pediatr Ophthalmol Strabismus 1990;27:315–16.
14.Olitsky SE, Kelly C, Lee H, Nelson LB. Unilateral rectus resection in the treatment of undercorrected or recurrent strabismus. J Pediatr Ophthalmol Strabismus 2001;38:349–53.
15.Retzlaff J, Paden PY, Ferrell L. Vector analysis of astigmatism. Adding and subtracting spherocylinders. J Cataract Refract Surg 1993;19:393–8.
16.Bagheri A, Farahi A, Guyton DL. Astigmatism induced by simultaneous recession of both horizontal rectus muscles. J AAPOS 2003;7:42–6.
17.Holladay JT, Moran JR, Kezirian GM. Analysis of aggregate surgically induced refractive change, prediction error, and intraocular astigmatism. J Cataract Refract Surg 2001;27:61–79.
18.Bartier M, Putteman A. Changes in astigmatism following surgery for strabismus (in French). Bull Soc Belge Ophtalmol 1988;229:87–96.
19.Snir M, Nissenkorn I, Buckman G, Cohen S, Ben-Sira I. Postoperative refractive changes in children with congenital esotropia: a preliminary study. Ophthalmic Surg 1989;20:57–62.
20.Fledelius HC, Christensen AC. Reappraisal of the human ocular growth curve in fetal life, infancy, and early childhood. Br J Ophthalmol 1996;80:918–21.
21.Clark RA, Demer JL. Posterior inflection of weakened lateral rectus path: connective tissue factors reduce response to lateral rectus recession. Am J Ophthalmol 2009;147:127–33.e2.