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Abstract

Extraocular disorders and their surgical management can significantly influence corneal astigmatism and higher-order aberrations (HOAs). This review aimed to evaluate the relationship between extraocular conditions, their surgical correction, and subsequent changes in corneal astigmatism and HOAs. A comprehensive literature search was conducted using PubMed, Scopus, and Web of Science, including studies published between 1992 and 2024. Search terms included astigmatism, eyelid surgery, thyroid eye disease (TED), orbital decompression, blepharoplasty, chalazion, dermatochalasis, ptosis, pterygium, scleral buckle, and HOAs. The reviewed literature demonstrates that a wide spectrum of extraocular disorders (such as ptosis, dermatochalasis, TED, chalazion, and pterygium) are associated with clinically significant changes in corneal astigmatism and HOAs. These alterations are affected by factors including lesion size, anatomical location, and the type of surgical intervention. For instance, ptosis surgery may either reduce or induce astigmatism depending on patient age and surgical technique, while chalazion excision and pterygium removal frequently lead to meaningful reductions in astigmatism and HOAs, particularly in cases involving larger lesions. The timing of postoperative evaluation and surgical approach plays a critical role in the magnitude and persistence of these optical changes. Awareness of the impact of extraocular diseases and their surgical treatment on corneal astigmatism and HOAs is essential for accurate interpretation of refractive changes, postoperative follow-up, and optimal patient management.

Plain language summary

How eye and eyelid conditions and their surgeries can change vision by affecting the front of the eye.

This article looks at how problems with the outer parts of the eye, such as the eyelids or tissues around the eye, can change the shape of the cornea, the clear front surface of the eye. When the cornea’s shape changes, it can cause vision problems such as blurriness or distortions. These problems are often related to astigmatism or higher-order aberrations, both of which affect how clearly a person sees. Some common conditions, such as droopy eyelids (ptosis), excess eyelid skin (dermatochalasis), thyroid-related eye disease, or growths like pterygium, can press on the eye and change the cornea’s shape. Even small lumps like chalazion, which result from a blocked oil gland in the eyelid, can distort the cornea. The good news is that surgery to treat these conditions often helps the cornea return to a more normal shape. This article reviews many scientific studies to examine how these conditions and their surgeries affect the cornea. In most cases, surgery leads to an improvement in vision by reducing astigmatism or other corneal distortions. However, the effects may vary depending on the patient’s age, the size of the lesion, and the surgical technique used. In some cases, surgery may temporarily worsen corneal changes before improvement occurs. Understanding these changes is important for eye care professionals, as it helps guide treatment planning and determine the appropriate timing for procedures such as cataract surgery or vision correction. The article recommends waiting several months after eyelid or pterygium surgery before performing procedures that rely on corneal measurements, to ensure that the eye has fully stabilized.

Keywords

astigmatism blepharoplasty chalazion eyelid surgery higher-order aberration ptosis

Introduction

The understanding of astigmatism originated in the early 1800s when Thomas Young documented his astigmatism. However, it was not until 1825 that George Airy became the first to utilize a cylindrical lens to correct his astigmatic refractive error.¹ A meta-analysis shows that astigmatism is the most prevalent refractive error in adults, with an estimated pooled prevalence of 40%.² Untreated astigmatism may lead to a significant deterioration in visual acuity and be associated with changes in visual and refractive development. Over the past two centuries, significant advances have been made in treating astigmatism and understanding its impact on the visual system.³

Ocular astigmatism occurs due to uneven curvature in the cornea (corneal astigmatism) or the crystalline lens (lenticular astigmatism). The combined effect of both determines the total astigmatism. Corneal astigmatism is classified by the axis as with-the-rule (WTR), against-the-rule (ATR), or oblique.¹ The exact cause of astigmatism is still unclear, but population studies have identified risk factors, including being under 12 months old, Hispanic or African American race, having major refractive errors (myopia or hyperopia), and maternal smoking during pregnancy.^4,5

Extraocular diseases can significantly affect the structures surrounding the eye, thereby influencing ocular movement, coordination, and alignment. Conditions such as eyelid ptosis, dermatochalasis, thyroid eye disease (TED), and chalazion can influence corneal astigmatism, despite not causing it directly.^6–8 For instance, chalazion can alter corneal shape, while eyelid ptosis can apply pressure on the cornea, especially in children, leading to astigmatic changes. Surgical interventions for these disorders, such as ptosis correction and chalazion excision, can also affect corneal astigmatism.^7–9

Wavefront analysis is a common method for measuring corneal higher-order aberrations (HOAs), helping to identify irregularities that affect vision. Types of HOAs include spherical aberration, coma, trefoil, and astigmatism, caused by factors like genetics, aging, eye injuries, and certain conditions. Extraocular diseases have also been linked to changes in HOAs.^10–12 HOAs of the cornea refer to irregularities in the shape of the cornea that can affect vision quality beyond what can be corrected with glasses or contact lenses. These aberrations can cause symptoms such as glare, halos, double vision, and poor contrast sensitivity. Many extraocular disorders and related surgeries can cause changes in HOAs, just as they can affect corneal astigmatism.^10–12

Despite the above-mentioned associations, there is a notable lack of comprehensive reviews on the impacts of extraocular diseases and their treatments on corneal astigmatism and HOAs, which this article aims to address.

Methods

In this narrative review, an extensive search was conducted in databases such as PubMed, Web of Science, and Scopus using relevant keywords. The search encompassed all available literature up to the date of the search. The full text of selected articles was thoroughly reviewed, and additional relevant studies were identified through manual searches of reference lists from the retrieved articles.

Studies were included if they evaluated the effect of extraocular diseases or their surgical management on corneal astigmatism and/or HOAs, involved human subjects, and were published in peer-reviewed journals between 1992 and 2024. Articles assessing eyelid disorders, TED, chalazion, pterygium, lower eyelid diseases, scleral buckling, or strabismus surgery with quantitative corneal measurements were eligible. Exclusion criteria included case reports with insufficient data, non-English publications, animal studies, conference abstracts without full text, and studies lacking objective corneal astigmatism or wavefront-related outcomes. Finally, 74 articles were included and reviewed (Figure 1).

Figure 1.

Study selection flowchart.

Results

Eyelid ptosis

Blepharoptosis, or ptosis, is a common eye disorder marked by the drooping of the upper eyelid due to dysfunction in the levator palpebrae superioris or Müller muscle. It can present as either congenital or acquired forms, leading to varying clinical manifestations, from mild cosmetic concerns to significant visual impairment. The causes of blepharoptosis can be diverse, including neurogenic, myogenic, aponeurotic, and mechanical factors.^12–17

Recent studies have increasingly highlighted the correlation between eyelid ptosis and corneal astigmatism. For instance, a nationwide survey in Taiwan found that children with ptosis are at a significantly higher risk for refractive disorders, reporting a 5.93-fold increased risk of astigmatism compared to their non-ptotic peers.¹⁸ Another cross-sectional study conducted on the Korean general population also showed that an increased positive spherical change and astigmatism incidence were prominent among ptotic participants younger than 60 years.¹⁹ This higher prevalence of astigmatism in patients with blepharoptosis can be justified by the results of a study by Ugurbas et al., in which they showed that eyes with congenital ptosis had an increased incidence of bow tie pattern on corneal topography and corneal asymmetry and irregularity. Interestingly, they also found a higher incidence of astigmatism.²⁰ In addition to astigmatism, Kumar et al. reported that eyes with congenital ptosis differed from their normal fellow eyes in the HOAs. They showed that total coma aberration correlated with margin reflex distance 1 (MRD1), defined as the distance between the upper eyelid margin and the corneal light reflex in primary gaze, in the ptotic eyes.²¹

In addition to ptosis itself, ptosis correction surgical methods can also lead to changes in corneal astigmatism. Mongkolareepong et al. observed a reduction in perioperative corneal astigmatism of up to 0.65 diopters (D) after levator resection in ptotic eyes with an initial astigmatism ⩾1.5 D. They even advised considering corneal astigmatism’s severity before planning cataract or refractive surgery in ptotic patients.²² Similarly, Savino et al. observed a decrease in corneal astigmatism of 0.26 ± 1.12 D with anterior levator complex tightening.²³ Regarding the time needed for the post-op correction of astigmatism, different studies reported different time periods. For instance, Yamamoto et al. observed a significant reduction in corneal astigmatism at 6 months postoperatively,²⁴ while Youssef et al. reported a 0.5 D decrease in corneal astigmatism at the 3-month follow-up, with no significant changes observed in the first month.²⁵ These findings indicate that at least 3 months is required to observe positive results of ptosis correction on astigmatism.

Another critical factor affecting the outcome of ptosis correction on astigmatism is age. Gandhi et al. found a decrease in corneal astigmatism of 0.47 ± 0.95 D at the 3-month follow-up after frontalis sling surgery in patients with congenital ptosis. They observed a steepening of the flatter meridians without significant change in mean keratometry, resulting in increased symmetry. However, their work’s considerable finding was that the changes in corneal astigmatism were more pronounced in children aged 5–10 years, possibly due to more remarkable plasticity. They also found that correcting ptosis at an earlier age was associated with improved visual acuity.²⁶

However, the correlation between astigmatism and ptosis surgery is controversial, as there were also reports of increased astigmatism in pediatric patients after ptosis surgery. In a study conducted on pediatric patients with blepharoptosis, Agrawal et al. showed a significant increase in corneal astigmatism of 0.43 D from 1.28 to 1.71 at the 3-month follow-up after sling surgery and levator resection.²⁷ Similarly, Cadera et al. reported increased corneal astigmatism in pediatric patients after surgery.²⁸ The study by Holck et al. showed that 86.2% of patients experienced an increase in corneal astigmatism after levator aponeurosis advancement via a transcutaneous approach. However, these changes were often transient and persisted in only two patients at 12-month follow-up.²⁹ These postoperative changes in corneal astigmatism may be due to patients’ hidden corneal astigmatism that becomes visible after surgical correction of ptosis.³⁰

Interestingly, it is worth noting that surgically induced corneal astigmatism of 0.78 ± 0.70 D and 0.82 ± 0.88 D were observed in age-related ptosis and contact lens-induced ptosis, respectively (Table 1).² Although previous studies indicate an increase in corneal astigmatism, it is important to note that these measurements are based on keratometry, which raises questions about the validity of these results.^28,29

Table 1.

Changes in total astigmatism following eyelid and pterygium surgeries.

Ocular condition	Author	Mean age	Eyes (n)	Surgery	Astigmatism changes
Blepharoptosis	Youssef et al.²⁵	24.7	30	Levator resection and sling	0.50 D reduction
	Cadera et al.²⁸	Pediatric	88	Levator resection and sling	0.30 D increase (In <4 years 0.20 D decrease)
	Paik et al.³²	15.1	108	Pentagonal sling	Changes in axis (toward the Oblique axis)
	Yamamoto et al.²⁴	72.6	32	Levator advancement	1.28 D reduction in anterior astigmatism and 0.61 D reduction in posterior astigmatism
	Holck et al.²⁹	62.2	29	Levator advancement	WTR astigmatism increase after 6 weeks that regressed to preoperative after 12 months
	Savino et al.²³	37.09	20	Levator tightening	0.26 D decrease
	Karabulut et al.³¹	31.5	28	MMCR	No significant changes
	Dannoue et al.⁷	68.24	108	Muller’s muscle tracking method	Astigmatic axis changed significantly in some patients
	Mongkolareepong et al.²²	51.97	42	Levator resection	0.65 D decrease if preop astigmatism ⩾ 1.5 D
	Agrawal et al.²⁷	Pediatric	30	Fasanella-Servat, sling, and levator resection	0.43 D increase
Pterygium	Errais et al.⁷⁸	49.3	20	Excision + LCAG	3.68 D decrease
	Bahar et al.⁸⁰	59.1	55	Bare sclera excision	0.61 D decrease
	Jain et al.⁷⁹	34.16	64	Excision + CAG	0.87 D decrease
	Maheshwari et al.⁶⁵	NA	151	Excision + CAG	2.85 D decrease
	Altan-Yaycioglu et al.⁷⁶	57.5	240	Excision + CAG, CRF, AMT	2.18 D decrease
	Gumus et al.⁸²	47.1	18	Excision + CAG and corneal polishing	0.2 D decrease
Chalazion	Sabermoghaddam et al.⁵⁸	28.7	14	Internal vertical incision	0.1 D decrease and 0.24 decrease in total HOAs
	Oncul et al.⁵⁷	24.9	36	Internal vertical incision	Some HOAs decrease significantly
	Bagheri et al.⁵⁶	31.14	228	Excision with internal or external approach	0.34 D decrease
	Park et al.⁵⁵	24	23	Internal vertical incision	Significant reduction (Astigmatism and HOAs) in lesions > 5 mm
					Insignificant reduction in lesions 3–5 mm
Dermatochalasis	Altin et al.³⁹	56.7	206	Blepharoplasty	0.22 D decrease
	Zinkernagel et al.⁴⁰	59	82	Ptosis surgery or blepharoplasty	Reduction in Ptosis: 0.25 D – in Blepharoplasty: 0.21 D (fat resection) and 0.9 D (skin only)
	Simsek et al.³⁸	46.3	43	Blepharoplasty	0.15 D increase
	Brown et al.³⁵	69.7	42	Blepharoplasty	Less than 1 D reduction in 89%
				Ptosis surgery	less than 1 D reduction in 70%
	Sommer et al.⁴⁴	65.4	42	Blepharoplasty	0.12 D increase
	An et al.⁴³	62.6	73	Blepharoplasty	No changes found
	Kim et al.⁴²	NA	50	Blepharoplasty or levator resection	Ptosis: decrease in 50% – Blepharoplasty: no changes in 66.6%
	Bhattacharjee et al.⁴¹	56.53	60	Blepharoplasty	0.19 D decrease
	Dogan et al.³⁷	56.5	60	Blepharoplasty	0.22 D decrease

AMT, Amniotic membrane transplantation; CAG, Conjunctival autograft; CRF, Conjunctival rotational flap; D, diopter; MMCR, Muller’s muscle-conjunctival resection; LCAG, Limbo-conjunctival autograft; LTS, Lateral tarsal strip.

There are also reports of no change in astigmatism in these patients. Karabulut et al. performed conjunctival Mueller’s muscle resection in patients with mild ptosis and found no significant change in corneal astigmatism at 3- and 6-month follow-ups.³¹ Paik et al. reported no significant changes in the magnitude of corneal astigmatism after pentagonal sling surgery; however, a considerable shift toward oblique corneal astigmatism was observed.³² In addition to the magnitude of astigmatism, the type change in astigmatism was also reported in patients undergoing ptosis surgery. For example, Dannoue et al. observed a change in the type of corneal astigmatism after Muller’s muscle tracking method, including shifts from oblique to WTR corneal astigmatism, WTR to oblique corneal astigmatism, and WTR to ATR corneal astigmatism.⁷

Dermatochalasis and blepharoplasty

Eyelid operations such as blepharoplasty are commonly performed worldwide in orbital and cosmetic surgery.³³ People with dermatochalasis may experience increased force on the eyeball due to overly droopy and weak eyelids, leading to potential changes in ocular metrics such as the anterior surface curvature and thickness of the cornea, corneal refractive power, and intraocular lens (IOL) power calculations.³⁴ The influence of upper eyelid pressure on corneal shape is well known. Previous research has shown that eyelid surgery alters the cornea’s curvature. Removal of the skin and reduction of the eyelid weight during blepharoplasty may lead to a redistribution of the pressure exerted by the eyelids on the cornea, resulting in changes in the cornea’s curvature and other corneal topographic properties.^35–38

Dogan et al. showed that upper eyelid blepharoplasty leads to an increase in the steepest corneal curvature after 3 months. However, this effect was only observed in individuals who had some degree of ptosis as indicated by an MRD1 of less than 2.5 mm. According to their results, no topographic changes were observed in subjects with MRD1 equal to or greater than 2.5 mm.³⁷ In a similar study, 1 month after blepharoplasty, the mean refractive astigmatism and HOAs significantly decreased by 0.22 and 0.07 D, respectively. Astigmatism change was higher in patients with MRD1 less than 2 mm than in cases with MRD1 equal to or greater than 2 mm.³⁹

Zinkernagel et al. found that upper eyelid surgery causes changes in corneal shape and refractive properties, especially in patients with severe upper eyelid abnormality. This study documented significant statistical changes in astigmatism after blepharoplasty. The significant change in corneal astigmatism in the group with resection of the large fat pads was observed (0.21 D) compared to the groups with skin-only blepharoplasty (0.09 D).⁴⁰ Brown et al. also observed a mean dioptric change of 0.55 D 3 months after blepharoplasty, as determined by keratometry measurements. Although only 11% of cases showed astigmatic changes of more than 1.00 D, they concluded that blepharoplasty may result in visually significant astigmatic changes in the cornea.³⁵ Another study showed that after blepharoplasty, the topographic cylinder values decreased by 0.19 D without changing the axis. This study reported that HOAs also decreased after surgery, which was not related to the removal of skin alone or skin with tissue. These changes were still present 1 year after surgery.⁴¹ However, in another study, conducted by Simsek et al., a significant increase of about 0.13 D in corneal astigmatism without axis change in patients after blepharoplasty was reported, but visual acuity changes were clinically insignificant.³⁸

On the contrary, there are also studies showing no significant change in astigmatism post-blepharoplasty. A study conducted by Kim et al. on corneal topography measurements of patients undergoing blepharoplasty showed that 6 weeks after blepharoplasty, corneal power, and astigmatism remain unchanged in most patients.⁴² Also, An et al. found that 3 months after blepharoplasty, which only involves skin removal, corneal astigmatism does not change.⁴³ Meanwhile, Sommer et al. reported that 1 month after removing only the skin in blepharoplasty, corneal astigmatism significantly increased by 0.12 D, but this change was not clinically valuable.⁴⁴

Interestingly, corneal optical changes were found to be procedure-specific, differing between blepharoplasty and ptosis repair. Significant reductions in astigmatism and HOAs were observed only after levator resection, not isolated blepharoplasty.⁴⁵ Moreover, the degree of ptosis correction correlated significantly with reductions in S3 and coma-like aberrations.⁴⁵

Thyroid eye disease

TED leads to symptoms such as eyelid retraction, eye misalignment, and proptosis.⁴⁶ Decreased visual acuity in TED may be attributed to corneal exposure keratopathy or compression of the optic nerve. However, in milder cases of vision loss in TED, corneal astigmatism could be a factor. It was previously shown that some of the topographic measures, including keratoconus prediction index, surface asymmetry index, simulated keratometry astigmatism, surface regularity index, inferior-superior index, and anterior instantaneous astigmatism axis, were significantly different between a group of control eyes and patients with TED.⁴⁶ It was shown that the anterior corneal astigmatism axis was more oblique in the TED group.⁴⁷

Thyroid dysfunction may lead to the accumulation of mucopolysaccharides in the corneal stroma and alter the shape of the cornea. Individuals with hyperthyroidism typically exhibit thinner corneas and more abnormal tomographic parameters that are associated with keratoconus.^48,49 Likewise, another study suggests correlations between thyroid gland dysfunction and keratoconus.⁵⁰

Moreover, Mombaerts et al. showed that Graves’ ophthalmopathy is linked to an increased WTR corneal astigmatism, causing newly induced visual acuity defects in 9% of patients with Graves’ ophthalmopathy, seemingly due to soft-tissue fibrosis in the superolateral orbital area.⁵¹

Iskeleli et al. also showed that orbital radiation in TED did not affect the corneal topography at 6- and 8-week follow-ups significantly, despite the reduction in extraocular muscle hypertrophy and edema.⁵² Kim et al. indicated that after orbital decompression surgery in patients with inactive TED, the steepest axis in the 3-mm zone underwent incyclotortion and the corneal astigmatism significantly altered, impacting the cornea’s optical function.⁵³

Chalazion

In particular, a large chalazion has a noticeable impact on corneal astigmatism due to the pressure being exerted on the cornea (Table 1).⁵⁴ The induced astigmatism is associated with the lesion characteristics, including size and location. Park et al. reported that after drainage of chalazia larger than 5 mm, induced corneal astigmatism is significantly reduced, but the reduction of astigmatism after the drainage of 3–5 mm chalazia is not statistically significant. Therefore, they recommended the removal of chalazia in cases of lesions greater than 5 mm to reduce corneal surface aberrations.^55,56

Bagheri et al. reported a statistically significant decrease in corneal astigmatism by 0.34 ± 0.35 D (p < 0.0001) after removal of the chalazion through an internal or external approach. Their results also indicated that chalazion lesions located in the upper eyelid exerted a greater influence on the induced corneal astigmatism. They showed that the reduction of corneal astigmatism after chalazion surgery depends on the type of chalazion. Thus, single, firm, and central lesions result in greater astigmatism reduction after drainage than multiple, soft, and peripheral lesions.⁵⁶

Oncul et al. also noticed that patients with chalazion had higher levels of corneal aberration and corneal densitometry values than healthy individuals. However, these values decreased following the surgical removal of the chalazion.⁵⁷ In line with this, a study by Sabermoghaddam et al. reported a significant reduction in HOAs after chalazion excision.⁵⁸

Lower eyelid disease

Lower eyelid diseases including ectropion, epiblepharon, and entropion have been shown to be associated with changes in corneal astigmatism. Considering the direct contact of the lower eyelid with the globe and the role of muscle tonicity in eyelid blinking, it is reasonable that the ocular surface is affected by lower eyelid diseases.^59,60 Additionally, the lateral tarsal strip procedure reduces eyelid laxity and usually increase the compressive effect of the eyelid on the cornea, which can cause a change in the amount and axis of astigmatism.

Detorakis et al. discovered that the regularity of astigmatism decreased significantly in eyes with lower eyelid ectropion compared to their fellow eyes. After surgery, the regularity of astigmatism and the percentage of eyes with WTR astigmatism significantly increased.⁶¹ In a study by Eshraghi et al., it was shown that the lateral tarsal strip procedure could lead to relevant changes in both the magnitude and axis of corneal astigmatism, with an axis change greater than 10° being sufficient to impact visual function within a 3-month follow-up period (Table 2).⁶²

Table 2.

Corneal astigmatism changes after extraocular surgeries.

Author	Intervention	Age (Years)	Change of astigmatism (Diopter)
Author	Intervention	Age (Years)	Before	After
Detorakis et al.⁶¹	Lateral tarsal strip procedure	72.44	1.87	1.41
Eshraghi et al.⁶²	Lateral tarsal strip procedure	82.6	1.62	1.60
Kim et al.⁶³	Epiblepharon surgery	NA	1.10	0.84
Yang et al.⁶⁴	Epiblepharon and entropion surgery	⩽7	1.8	1.9
		>7	2.1	2.1
Kim et al.⁵³	Orbital decompression surgery (TED)	~47	0.96	0.94
Mombaerts et al.⁵¹	Orbital, strabismus, and/or eyelid surgery in TED patients	<55	Higher than controls (~3.0–3.25 D)	No significant change
Cetin et al.⁸⁹	Encircling scleral buckling surgery	55.8	3.7	3.1
Bedarkar et al.⁹³	Scleral buckling	16–30	0.51	2.04
		31–45	2.05	3.18
		46–60	1	2.56
Lee et al.⁹⁷	Horizontal rectus muscle surgery (R&R) for intermittent exotropia	9.55	1.37	1.65
Karakosta et al.⁹⁴	Unilateral horizontal rectus recession (medial or lateral)	5.5	Postoperative increase in corneal astigmatism (≈ +0.47 D at 6 weeks)

Kim et al. examined the impact of epiblepharon surgery on visual acuity and WTR astigmatism in children compared to those who did not undergo surgery. They found a significant reduction in astigmatism after surgical correction in patients with epiblepharon, particularly in those with higher baseline levels of astigmatism. They recommended considering epiblepharon surgery for patients with high levels of astigmatism.⁶³ Also, Yang et al. investigated changes in astigmatism before and after surgery in patients with epiblepharon and congenital entropion. They reported no significant difference in corneal astigmatism changes following surgery between patients under the age of 7 and those over the age of 7.⁶⁴

Pterygium

The grade of pterygium correlates with the severity of corneal astigmatism, with higher grades being associated with greater astigmatism.^65,66 Also, HOAs tend to be higher in eyes with pterygium compared to normal fellow eyes; in many cases, it is correlated with the size of the pterygium.⁶⁷ Several studies demonstrated that nasal pterygium significantly induces hemi-meridional WTR corneal astigmatism, corneal irregularity, and some HOAs.

The pterygium grade, length, width, site, and increase in vascularity impact the magnitude of astigmatism. For instance, when the primary pterygium extends beyond 1.0 mm from the limbus, it causes noticeable astigmatism of 1.0 D or greater in the WTR direction, and the increased limbal thickness of pterygium leads to more refractive astigmatism.^68–73

Despite the above findings, the topographic changes of the cornea that are caused by the pterygium are mostly reversible after pterygium removal.⁷⁴ These changes are linked to the preoperative size of the pterygium and the preoperative astigmatism.^75,76 Pterygium excision significantly reduces corneal wavefront aberrations in both primary and recurrent pterygium, with a more effective reduction observed in the primary form.⁷⁷

Many studies have investigated the amount of corneal astigmatism reduction after pterygium surgery with different techniques. The three main surgical techniques for removing pterygium are bare sclera, conjunctival autograft, and amniotic membrane graft. All of these methods have been shown to significantly decrease corneal astigmatism. However, the bare sclera technique is less effective than the other methods in reducing astigmatism, and no significant difference is reported between the efficacy of conjunctival autograft and amniotic membrane graft surgery.⁶⁶

Errais et al. showed that the corneal topographic changes caused by the pterygium were almost reversed after excision. The corneal astigmatism decreased from 5.47 D to 1.79 D after limbo-conjunctival autograft surgery.⁷⁸ Jain et al. observed a significant reduction in corneal astigmatism from 1.37 D to 0.50 D after autologous conjunctival graft surgery.⁷⁹ Maheshwari reported a significant reduction in corneal astigmatism from 4.40 D to 1.55 D after conjunctival autograft transplantation surgery.⁶⁵ Moreover, it was shown by another study that following five different surgical techniques for pterygium, including conjunctival autograft with sutures, fibrin glue, conjunctival rotational flap, amniotic membrane transplantation with suture or with glue, mean corneal astigmatic values significantly decreased from 3.47 D to 1.29 D.⁷⁶ Bahar et al. reported that corneal astigmatism decreased from 3.12 D to 2.51 D after excision by bare sclera technique combined with mitomycin, accompanied by improvements in surface regularity index, surface asymmetry index, and visual acuity.⁸⁰

Niruthisard et al. reported that 40% and 73% of patients reached corneal astigmatic and keratometric stability, respectively, in 6 months of follow up. A longer waiting duration after surgery is recommended for stabilizing pterygia greater than 3 mm.⁸¹ In line with this, Gumus et al. suggested that the decrease in postoperative aberrations persisted beyond the initial postoperative period, extending up to 1 year after surgery. As a result, they recommended delaying any refractive procedures for at least 1 year following pterygium surgery to allow for corneal stability (Table 1).⁸² Similarly, Narasimhaiah et al. indicated that the use of polishing after pterygium surgery with a diamond burr improves the correction of corneal astigmatism compared to manual polishing at 6 months.⁸³

New studies have tried to identify ways to predict reductions in astigmatism and HOAs, suggesting preoperative astigmatism greater than 1.42 D (area under the curve (AUC) = 0.934) predicts more than half of the reductions in astigmatism after pterygium excision.⁸⁴ It also suggests astigmatisms greater than 3.60 D (AUC = 0.946) and horizontal invasion length (HIL) greater than 3.34 mm predict more than half of reduction in root mean squares (RMS) of low-order aberrations and HOAs, respectively.⁸⁴ Additionally, for predicting postoperative residual astigmatism greater than 1.25 D, thresholds of astigmatism greater than 5.78 D and HIL greater than 5.03 mm were identified.⁸⁴

Another recent study examined corneal steep islands (CSIs) after pterygium surgery with conjunctival-limbal autografts. CSIs occurred in 28% of eyes and were associated with significantly elevated higher-order RMS aberrations postoperatively.⁸⁵ Interestingly, CSIs were predicted based on higher preoperative astigmatism, higher HIL, lower pterygium height, and residual corneal thickness to central corneal thickness (RCT/CCT) ratio.⁸⁵

Scleral buckling

Scleral buckling is a commonly used procedure for the treatment of retinal detachment. However, despite retinal reattachment, patients are occasionally dissatisfied with the results. This dissatisfaction can be attributed to changes in the general characteristics of the cornea, including changes in astigmatism, myopia, and topographic features after surgery.^86,87

Ornek et al. reported that the transient changes in corneal astigmatism and myopia observed after scleral buckle surgery resolve after 6 months.⁸⁸ Cetin et al. also reported these transient changes; corneal astigmatism increased significantly 1 week after surgery but gradually decreased to 4.3 D, 3.3 D, and 3.1 D after 1 week, 1 month, and 3 months, respectively.⁸⁹

Okamoto et al. documented an increase in HOAs 2 weeks, 1 month, and 3 months postoperatively. Notably, segmental buckling showed a more pronounced effect on corneal aberrations compared to the encircling group.⁹⁰ Lee et al. similarly observed an increase in HOAs in patients with rhegmatogenous retinal detachment who underwent scleral buckling.⁹¹

The induced corneal astigmatism was found to be related to the distance of the buckle from the limbus.⁹² Moreover, Bedarkar suggested that these changes varied among different age groups, as in the older patients the surgically induced astigmatism resolved earlier compared to that of younger patients.⁹³

Strabismus

Strabismus is most commonly corrected via horizontal rectus muscle surgery.⁹⁴ The refractive effects of these surgeries have been studied in both pediatric and adult populations.

Karakosta et al. reported a statistically significant 0.43 D increase in corneal astigmatism following unilateral horizontal rectus muscle recession in children, observed 6 weeks post-operatively. This increase, particularly in patients with pre-existing WTR astigmatism or no astigmatism, was attributed to alterations in ocular surface tension and muscle insertion point changes. Consequently, the authors recommended when both eyes have comparable vision, and one eye has WTR or no astigmatism, horizontal rectus recession should ideally be performed on the other eye.⁹⁴

Moon et al. corroborated these findings, demonstrating a 0.25 D increase in WTR astigmatism in operated eyes following unilateral strabismus surgery for intermittent exotropia, while spherical equivalent refractive error remained unchanged. Age, gender, and preoperative refractive error did not correlate with postoperative astigmatism changes; however, surgical technique significantly influenced outcomes.⁹⁵ One study reported an initial increase in astigmatism at 1 week, followed by a decrease at 3 months, without a return to baseline.⁹⁶

In children undergoing horizontal rectus muscle surgery for intermittent exotropia, one study observed a statistically significant increase in WTR astigmatism and a myopic shift in spherical equivalent. Stabilization occurred within 3 months post-operatively, emphasizing the need for refractive evaluation and correction after this period.⁹⁷

Conversely, other research indicated that while transient refractive changes are common post-operatively, statistically significant shifts often lack clinical relevance and resolve over time.⁹⁸ Specifically, horizontal muscle surgery induces a temporary myopic shift due to transient axial length elongation and corneal astigmatism changes, which typically resolve to preoperative levels within 1 month and remain stable throughout the follow-up period (Figure 2).⁹⁹

Figure 2.

Schematic summary of mechanisms leading to corneal astigmatism and HOAs changes in extraocular diseases and related surgeries.

Clinical implications

The findings of this review have several important clinical implications for both diagnostic evaluation and surgical decision-making. Awareness of extraocular disease–related and surgery-induced changes in corneal astigmatism and HOAs can assist ophthalmologists in optimizing preoperative planning, selecting appropriate surgical timing, and accurately interpreting postoperative visual complaints that may not be explained by standard refraction alone. These effects are particularly relevant in patients undergoing cataract surgery, refractive procedures, or IOL power calculations, where unrecognized corneal instability or transient astigmatic changes may result in refractive surprises and patient dissatisfaction.

Furthermore, understanding the potential reversibility or progression of corneal changes following extraocular surgery can help clinicians determine appropriate waiting periods before definitive refractive interventions. Incorporating advanced diagnostic tools such as corneal tomography and wavefront aberrometry into routine clinical assessment may enhance the detection of subtle corneal shape alterations and HOAs that are not captured by keratometry alone. This approach may improve patient counseling, guide follow-up strategies, and ultimately contribute to better visual quality, contrast sensitivity, and overall postoperative outcomes.

Limitations

This review has several limitations. First, the included studies were heterogeneous in terms of study design, patient demographics, types of extraocular diseases, surgical techniques, and outcome measures, which limits direct comparison across studies and precludes quantitative synthesis. Second, many studies primarily relied on keratometry-based measurements rather than comprehensive corneal tomography or wavefront aberrometry, potentially underestimating subtle corneal irregularities and HOAs. Third, a substantial proportion of the available evidence consisted of retrospective studies with relatively small sample sizes and limited long-term follow-up, reducing the ability to assess the persistence and clinical significance of postoperative corneal changes over time. In addition, variability in the timing of postoperative assessments across studies may have affected the reported magnitude and stability of astigmatism and HOAs changes. Finally, potential publication bias and the underrepresentation of negative or neutral findings may have influenced the overall conclusions drawn from the literature.

Conclusion

Overall, these findings highlight the multifactorial nature of corneal astigmatism and HOAs. Individualized preoperative planning and postoperative assessment are essential when managing corneal astigmatism across various extraocular surgical interventions. In most cases, corneal instability requires 3 months to 1 year to stabilize; therefore, refractive surgery or IOL power calculations should be postponed until corneal stability is documented. We recommend more standardized, prospective studies to compare the effects of different surgical techniques on corneal astigmatism and HOAs. Additionally, the use of corneal tomography and wavefront aberrometry for reliable and consistent outcome measurements is highly recommended. Wavefront aberrometry, in particular, was underutilized in many studies included in this review, despite evidence that reductions in HOAs may improve contrast sensitivity and overall visual function beyond numerical refractive outcomes.

Footnotes

Acknowledgements

None.

Declarations

ORCID iDs

Hassan Asadigandomani

Mohammad Soleimani

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Exploring the impact of extraocular disorders and their surgical correction on corneal astigmatism and higher-order aberrations: a comprehensive review

Abstract

Plain language summary

Keywords

Introduction

Methods

Results

Eyelid ptosis

Dermatochalasis and blepharoplasty

Thyroid eye disease

Chalazion

Lower eyelid disease

Pterygium

Scleral buckling

Strabismus

Clinical implications

Limitations

Conclusion

Footnotes

Acknowledgements

Declarations

ORCID iDs

References