Management of Post-LASIK Ectasia

Partha  Biswas; Sneha  Batra

Management of Post-LASIK EctasiaCHAPTER 1

Partha Biswas,

Sneha Batra

INTRODUCTION

Laser-assisted in situ keratomileusis (LASIK) has become the gold standard for the treatment of refractive errors worldwide.¹ Over time, the rate of complications has been seen to be extremely low.² However, when these complications do occur, visual consequences can be substantial and patient dissatisfaction high, particularly because it is performed mainly as an elective cosmetic procedure, especially in young patients.

Post-LASIK ectasia (PLE) is defined as a region of abnormal steepening and increased curvature within a centrally flattened optical zone.³ There is associated biomechanical weakening of the cornea.⁴

Seiler documented the first case report of PLE in the year 1998,⁵ and it was thought at that time that an epidemic of iatrogenic keratectasia is looming over the world with increasing numbers of refractive procedures being performed worldwide without proper screening criteria in place. However, 20 years down the line, that fear has not been substantiated, and rate of PLE reported has remained low worldwide.^6,7

Prevention and management of post-LASIK ectasia has remained a hot topic for debate, and following a famous trial in 2005 when a young man with PLE was awarded millions of dollars as compensation, a consensus group was formed by American Academy of Ophthalmology (AAO) and American Society of Cataract and Refractive Surgery (ASCRS), which enumerated the risk factors for eliminating high-risk candidates, and also certified that PLE may even occur in candidates without any known risk factor, and that it should not be considered negligence on part of the surgeon.⁸

EPIDEMIOLOGY

The incidence of PLE has been reported as 0.01–0.66% in various studies.^6,7 The mean duration from the initial laser procedure to detection is 15.3 months. A quarter of patients develop PLE within the first 3 months and at least half of them within 1 year of the laser procedure.⁹ The earliest case was reported within one week,¹⁰ while the latest was after 144 months.¹¹2

Post-LASIK ectasia was seen more frequently among males and in the younger age group, in patients with thin corneas and high refractive errors pre-operatively.⁹

PRESENTING FEATURES

Any case of post-LASIK myopic regression, particularly if accompanied by a change in corneal topography, should be regarded with suspicion. Such patients should be closely followed up for at least 6 months before a decision for an enhancement procedure is taken.

Common Clinical Findings

Progressively increasing refractive error (mainly myopia and irregular myopic astigmatism).
Progressively decreasing best corrected visual acuity (BCVA).
Stromal thinning (Fig. 1).
Anterior and posterior corneal steepening.
Vogt's striae (rarely).

Rare presentations in PLE include acute hydrops with perforated cornea,¹² and a case of globe rupture secondary to trauma.¹³

INVESTIGATIONS HELPFUL IN THE DIAGNOSIS OF PLE

Corneal topography (Figs. 2A to D).
Anterior segment optical coherence tomography (AS-OCT) showing ectatic changes (Fig. 3).
Ocular response analyzer (ORA) shows decreased ocular hysteresis.¹⁴

Randleman criteria for PLE is as follows:¹⁵

Inferior topographic steepening of more than or equal to 5 diopters (D).
Loss of more than or equal to 2 Snellen's lines of visual acuity.
Alteration in refractive error of 2 D (spherical or cylindrical).

Fig. 1: Slit lamp photograph of a patient with post-laser-assisted in situ keratomileusis ectasia showing stromal thinning, ectasia, and scarring.

Figs. 2A and B:

Padmanabhan et al. in their study suggested the following criteria as indicators of development of post-LASIK ectasia:¹⁶

Increasing myopic refractive error with decrease in BCVA.
An increase in magnitude of the highest anterior and posterior topographic elevation.4

Figs. 2A to D: Corneal topography of a patient with post- laser-assisted in situ keratomileusis ectasia. (A and B) Refractive quad map of right and left eyes showing ectatic changes; (C and D) Belin/Ambrósio enhanced ectasia display of the same patient showing ectatic changes.

Fig. 3: Anterior segment optical coherence tomography of a patient with post-laser-assisted in situ keratomileusis ectasia showing thinning and ectatic changes.

A shift of the location of the steepest point on the anterior cornea and that of the highest elevation of the posterior cornea towards the center of cornea.
A reversal of the corneal asphericity towards greater prolateness.
An increase in negative spherical aberration and coma.

They also devised a grading system for the management of PLE (Table 1).

RISK FACTORS FOR PLE

In their historic study,⁹ Randleman et al. described the major etiological factors for PLE, and also devised the ectasia risk score system (ERSS) to identify the high-risk candidates before the laser procedure (Table 2).

Preoperative Topographic Pattern

In the overall subgroup analysis in the Randleman study, abnormal topography pattern was found to be the most significant factor. More than 40% of ectasia cases had grossly abnormal changes such as keratoconus and pellucid marginal degeneration (PMD).⁹ These are now considered to be absolute contraindications to LASIK with medicolegal implications (Fig. 4).

The following corneal topography patterns were considered:

Normal or symmetrical
Suspicious:
- Asymmetric bow-tie:
  - Asymmetric steepening less than 1 D
  - No skewing of radial axis (SRA)
- Inferior steep axis or SRA:
  - Significant SRA ± inferior steepening
  - More than or equal to 1 D of inferior steepening locally, but overall inferior-superior asymmetry (I-S) value less than 1.4.
Abnormal: Keratoconus, PMD, or forme fruste keratoconus with an I-S value of more than or equal to 1.4.

Residual Stromal Bed

Patients with PLE have been shown to have significantly lower residual stromal bed (RSB) thickness than controls.6

Table 1 Padmanabhan et al. grading system for post-LASIK ectasia.¹⁶

Grade	Normal	Mild	Moderate	Severe
Score	1	2	3	4
CDVA	≤0.18	0.19–0.48	0.49–0.78	>0.78
SE	+1 to –1	– 1.1 to –5	– 5.1 to –10	>–10
HPE	≤25	26–50	51–75	>75
Z°₄	≥0	<0 to ≥–0.5	<–0.5 to ≥–1	<–1
Q	≥0	<0 to ≥–1	<–1 to ≥–2	<–2
(CDVA: corrected distance visual acuity; HPE: highest posterior elevation; Q: corneal asphericity; SE: spherical equivalence; Z°₄: Zernike coefficient for spherical aberration)

Table 2 Randleman's ectasia risk factor score system (ERSS).⁹

Score	IV	III	II	I	0
Parameter
Corneal topography	Forme fruste keratoconus	Inferior steepening/skewed radial axis		Asymmetric bowtie	Normal/symmetric bowtie
Residual stromal bed (µ)	<240	240–259	260–279	280–299	>300
Age (years)		18–21	22–25	26–29	>30
Preoperative pachymetry (µ)	<450	451–480	481–510		>510
Preoperative refractive error (D)	>–14	>–12 to –14	>–10 to –12	>–8 to –10	– 8 or less

It has been studied that posterior stroma is biomechanically weaker as compared to the anterior stroma, due to the differential distribution of keratocytes. Hence, corneal tensile strength is seen to decrease after LASIK.

In the Randleman ectasia score, all RSB thickness values less than 300 µ were considered increasingly significant in 20 µ intervals. Moreover, it has been documented that up to 33% of eyes with attempted RSB thickness of 250 µ could end up having actual RSB thickness less than 200 µ. The variability of flap thickness has been seen to occur with both mechanical microkeratomes and femtosecond lasers. Hence, it is now said that intraoperative measurement of RSB thickness is critical. It was seen in a survey among members of the International Society of Refractive Surgery or AAO in 2004, that only 31% refractive surgeons routinely measure flap or RSB thickness during surgery.¹⁷

It is seen that ectasia due to low RSB thickness usually occurs in the central corneal region while inferotemporal ectasia is usually seen in missed cases of forme fruste keratoconus or PMD.¹⁸7

Fig. 4: Corneal topography showing ectatic changes suggestive of keratoconus—absolute contraindication for refractive surgery.

Why 250μ of RSB was Considered the Magical Cut-Off Number?

Andreasson et al.¹⁹ found the elastic modulus of the keratoconic cornea to be 1.6–2.5 (average 2.1) times less than that of a normal cornea. Using these data, Seiler et al.⁵ postulated that reduction in the load-bearing portion of a normal cornea from 525 µ to 250 µ (a factor of 2.1) might simulate the elasticity of a cornea with keratoconus and predispose to development of ectasia. This value coincides with Barraquer's early recommendation that a RSB thickness of at least 250 µ be maintained to prevent corneal ectasia after keratomileusis.²⁰

Age

When ectasia cases with and without topographic abnormalities were compared, age was the only other significantly different factor. Patients without abnormal topographies were significantly younger than patients with defined topographic abnormalities. In the Randleman study, patients younger than 30 years were seen to be at risk; however, no recommendation was made on the basis of age.

Preoperative Pachymetry

The refractive error, preoperative pachymetry and RSB are interdependent factors. In the ectasia score, corneas with less than 510 µ were considered to be at risk.8

High Myopia

In the Randleman study, patients with more than 8 D myopia were considered to be at risk. Pallikaris et al. had shown in their review that no subjects with a correction of less than –8 D or RSB more than 325 µ experienced ectasia.⁷ However, Amoils et al.²¹ showed that even low to moderate myopia between –4 D and –7 D could lead to PLE in the presence of other risk factors.

Condon et al.²² also showed that high myopia is not a risk factor provided other parameters are within normal limits. It may be that higher refractive error is mainly responsible for a lower RSB, which is the actual culprit for PLE.

Randleman's ectasia risk score was formulated using the above 5 parameters. It was shown to have 91% sensitivity and 96% specificity, and till date, it is used as the most reliable score to identify high-risk patients prone to develop PLE.

However, these risk factors are not absolute, and even after screening out high-risk patients based on this score, there is still a substantial percentage of patients developing PLE without seemingly being at risk. This has led to a number of other risk factors being postulated by other researchers such as:

Percent tissue altered (PTA): It is a novel metric devised by Santhiago et al.^23,24 which predicts high-risk patients irrespective of their topographic patterns. It is calculated as:

PTA = (FT + AD)/CCT, where FT: flap thickness; AD: ablation depth; CCT: central corneal thickness.

They showed that in a patient with normal corneal topography, PTA more than or equal to 40 was the most prevalent risk factor (97%), followed by age less than 30 years (63%), RSB less than or equal to 300 µ (57%) and Randleman ectasia score more than or equal to 3 (43%).

Compared to RSB or CCT values, PTA provides a more individualized measure of biomechanical alteration because it considers the relationship between total thickness, tissue altered through ablation and flap creation, and ultimate RSB thickness. PTA was shown to have higher prevalence, higher odds ratio, and higher predictive capabilities for ectasia risk than moderate to high ectasia risk score system values.

Ablation ratio: Brenner et al.²⁵ devised a new metric, ablation ratio, which is calculated as:

Ablation ratio = Ablation depth/Pachymetry

It was shown to have the strongest correlation with post-LASIK ectasia spherical equivalence.
Ablation depth: The depth of ablation and increased intraocular pressure (IOP) were shown to be significant risk factors for post-LASIK ectasia in white rabbits.²⁶ Tatar et al.²⁷ also showed that deep ablation more than 75 µ is the most important risk factor for the development of PLE.
Choice of procedure: About 4% cases of PLE have occurred after photorefractive keratectomy (PRK), whereas 96% cases occur after LASIK.⁹ Dawson et al.²⁸ reported that PRK, sub-Bowman's keratomileusis (SBK) and advanced surface ablation (ASA) cause lesser reduction in the biomechanical strength of the cornea.9
Multiple enhancements: Multiple ablations are also thought to be an associated factor.²⁹ However, it is difficult to say whether it is a true risk factor or the progressive myopia in these cases was actually due to missed cases of early PLE.
Thicker flaps: Thicker flap weakens the biomechanically crucial obliquely-oriented anterior stromal layer predisposing to PLE.³⁰
Chronic rubbing of eyes: It could be a contributory factor.³¹
Pregnancy: It may induce certain hormonal changes such as production of the hormone relaxin which can induce or exaggerate pre-existing PLE.³²
Other risk factors: These include candidates with family history of keratoconus and male sex.

Belin/Ambrósio Enhanced Ectasia Display (BAD)³³

Brazilian ophthalmologist Renato Ambrósio and Arizona's Michael Belin developed a new software incorporated in the Pentacam® machine, which uses imaging of both the anterior and posterior corneal surfaces, and uses elevation-based tomographic data, combined with pachymetric analysis to generate a more accurate screening criteria for refractive surgery. While the first set of images displays the elevation of the anterior and posterior surfaces of the cornea compared to the best fit sphere (BFS) over a central 8 mm zone, the second set of images (the enhanced elevation map) eliminates the ectatic portion of the cornea from the computation, which helps to accentuate the effect of ectasia even in minimal amount.

The lower two maps (subtraction maps) show a color coding (red/yellow/green) to differentiate between normal and ectatic corneas. The corneal thickness spatial profile (CTSP) and percentage thickness increase (PTI) graphs depict the progressive thinning of the cornea from the periphery to the thinnest point, and the percentage of increase from the thinnest point out to the periphery respectively. Ultimately, a D value (Belin-Ambrósio deviation value) is calculated, which is indicated in yellow (suspicious) when it is more than or equal to 1.6 standard deviation (SD) from the mean (Fig. 5A), and in red (abnormal) when it is more than or equal to 2.6 SD from the mean (Fig. 5B).

However, despite screening protocols with all the known risk factors in place, some patients still develop ectasia with no identifiable cause. It is now thought that an individual's intrinsic tensile strength of the cornea probably is the most crucial factor for the development of ectasia.^34–37

PATHOGENESIS

Post-LASIK ectasia can be said to occur when the tensile strength of an individual's cornea is lowered below a certain threshold which is essential to maintain the shape of the cornea. This can occur in the following three ways:³⁸

The cornea undergoing laser refractive procedure does not show any topographic changes, but is intrinsically weaker and prone to develop ectatic changes in the future.10

Figs. 5A and B: Belin/Ambrósio-enhanced ectasia display map. (A) Belin “suspicious” with D value in yellow range; (B) Ectatic changes with D value in red range.
The cornea undergoing laser shows subtle topographic changes, but seems to be stable clinically, and is weakened further by the laser procedure.
The cornea undergoing laser was biomechanically normal preoperatively, but an excessive amount of tissue loss weakens it beyond its threshold.

11The chief alteration predisposing to PLE is seen in the anterior corneal biomechanics which precipitates thinning and compression of collagen fibrils, resulting in loss of global structural integrity.⁶

HISTOPATHOLOGY

Randleman et al.³⁹ described in detail the histopathological and ultrastructural changes in corneas affected by PLE. Specimens of cornea with PLE which underwent penetrating keratoplasty (PKP) were observed for histopathological changes under light microscopy, and the following features were observed:

Corneal epithelial hypoplasia.
Breaks in the Bowman's membrane, typically smaller than that seen in keratoconus.
Adequate thickness of the flap.
Adequate thickness of the hypocellular primitive stromal scar.
Reduced thickness of the RSB.
Large interlamellar clefts in the ectatic region of the RSB.

The specimens were also evaluated in 2.5% glutaraldehyde under transmission electron microscope (TEM), where the following changes were noted:

Reduced thickness of the stromal lamellae.
Reduced number of lamellae in the stroma.
Loss of keratocyte density.⁴⁰
Reduced thickness of the collagen fibrils.⁴¹
Presence of aggregated microfibrils in the Bowman's membrane and stroma.
Degeneration of the proteoglycans within the collagen fibrils, which lead to degeneration of the fibrils themselves, causing disorganization of the lamellae.⁴¹
Wavy and distorted stromal collagen bundles, especially in the posterior corneal region.⁴²

Immunohistochemistry and Other Novel Investigations

Increase in proteinases such as matrix metalloproteinase (MMP) 10 and 3 suggesting ongoing epithelial basement membrane lysis and remodeling.⁴³
Alpha 1-proteinase inhibitor (α1-PI) and Sp1 expression are unchanged.⁴⁴
In vivo confocal microscopy shows increased corneal dendritic cell density.
Tear cytokine analysis shows altered cytokines as in dry eye suggesting a possible inflammatory role in PLE.⁴⁵
Significant elevation of MMP 9 and decrease in tissue inhibitor of MMP (TIMP) 1 in tear samples.⁴⁶

Biomechanical Elasticity Theory¹⁴

The biomechanical theory postulates that interlamellar and interfibrillar slippage occurs postoperatively in those areas of the residual stroma which 12are subjected to maximum stress. This chronic phenomenon is termed as “interfiber fracture”.

Guirao, in his study, used the spherical thin-shell model to demonstrate that tissue removal from an intact cornea causes anterior shifting of the posterior corneal surface with an increase in its dioptric power.⁴⁷

As mentioned earlier, the posterior cornea is biomechanically weaker as compared to the anterior stroma. The creation of an anterior flap disturbs this distribution as this vital part of the stroma no longer contributes to the biomechanical integrity of the cornea.²³

MANAGEMENT

Contact Lenses

Contact lenses can be used in the earlier stages of PLE. Rigid gas permeable (RGP) lenses are the most commonly used lenses. They are very similar to those used in keratoconus patients, and lenses are custom made for every patient.⁴⁸

Rose K lenses have been specially developed for ectatic corneas, and are now one of the most commonly used lenses worldwide (Fig. 6A). Scleral lenses have also been used in PLE patients, especially for those with irregular corneas (Fig. 6B).⁴⁹ They can be either semi-scleral (16–18 mm diameter), or full scleral lenses (18–22 mm diameter). Hybrid lenses with central RGP like features, and peripheral soft lens-like configuration, have also been developed, which have replaced piggyback lenses now (Fig. 6C). PROSE (prosthetic replacement of ocular surface ecosystem) lenses have also been tried successfully (Fig. 6D).⁵⁰

Collagen Cross-Linking (CXL)

Collagen cross-linking is considered to be the gold standard treatment for progressive corneal ectasia, but it is associated with slow and painful recovery periods.⁴

The indications for CXL in case of PLE are as follows:

Increase in K_max more than 1 D in 1 year.
Decrease in BCVA.
Requirement for altered contact lens fitting more than biannually.

The contraindications to CXL are as follows:

Thinnest pachymetry less than 400 µ.
Corneal infection.
Autoimmune diseases.
Pregnancy or lactation period.

The CXL protocol followed usually is the Dresden protocol⁵¹ which includes:

Removing the corneal epithelium over 8 mm under topical anesthesia.
Soaking the corneal stroma in isotonic 0.1% riboflavin solution every 3 minutes for 30 minutes.
Application of ultraviolet A light at 3 mW/cm² irradiance and 5.4 J/cm² dose for half an hour (Fig. 7).13

Figs. 6A to D: Contact lenses used in the management of post-laser-assisted in situ keratomileusis ectasia. (A) Rose K lens; (B) Scleral lens; (C) Hybrid lens; (D) PROSE lens.

Fig. 7: Collagen cross-linking for management of post-laser-assisted in situ keratomileusis ectasia.

Application of bandage contact lens for 3 days for rapid re-epithelialization.
Antibiotic and steroid eye drops are given postoperatively.

Collagen cross-linking has shown long-term stability without significant side effects, and over time, it improves BCVA, decreases cylindrical power and K_max values, and halts progression of topographic indices and higher order aberrations.^6,52,53 Confocal microscopy performed 1 year after CXL showed good results with no substantial alteration in the endothelial cell count.⁵⁴

However, compared to keratoconus eyes, the gain in BCVA is slow and usually not seen until 12 months after the procedure.⁵⁵ This is because cross-linking results in strengthening mainly of the anterior part of stroma, which is already compromised due to the creation of flap in a LASIK patient.⁵⁶

Various modifications of CXL to the original protocol have been tried to increase the efficacy in PLE patients:

Epithelium on CXL.⁴
Under flap CXL (ufCXL): early onset mild cases of PLE treated by lifting the LASIK flap and irradiating with 18 mW/cm² UV light.⁵⁷
Athens protocol: Consecutive sequential topography-guided partial transepithelial PRK and CXL.^58,59
Combined PTK-PRK-CXL (Cretan protocol plus) has also been successfully used to stop the progress of PLE.⁶⁰

Intracorneal Ring Segments (ICRS)

Various ICRS such as Intacs, Ferrara rings and Kera rings have been used successfully in the management of PLE (Figs. 8A to C).^61–63 These implants flatten the central portion of the cornea thereby reducing myopia. Its efficacy has been found to be directly proportional to the thickness of the segment, and inversely proportional to its diameter. The progression of PLE is often halted and a corneal transplant may no longer be required. The advantages are that it is reversible and tissue saving in nature.15

Figs. 8A to C: Intracorneal ring segments used in the management of post-laser-assisted in situ keratomileusis ectasia. (A) Intacs; (B) Ferrara rings; (C) Kera rings.

The indications of ICRS are:

Patients with loss of more than or equal to 2 Snellen's lines of BCVA.
Grade 4 PLE.

Contraindications to ICRS implantation are:

Any previous ocular surgery.
Vernal keratoconjunctivitis.16
Viral keratitis.
Pregnancy/lactation period.

The complications seen with ICRS are:⁶²

Intraoperative: Segment decentration, insufficient depth of channel, superficial dissection with perforation of Bowman's membrane
Postoperative: Extrusion of implant, neovascularization, infective keratitis, segment migration, melting of cornea

For PLE, implantation of a single segment in the ectatic portion is more effective in reducing the refractive error than implanting two segments.⁶⁴

Combination of ICRS and CXL has been tried successfully for vision improvement as well as stabilization of ectasia.⁶⁵

A new variety of ICRS known has Intacs SK (severe keratoconus) has been used in advanced cases of PLE with good results.⁶⁶

Keratoplasty

Corneal transplant is used as a last resort in cases with intolerance to RGP lenses, and unacceptable BCVA, usually having contraindication to CXL or ICRS. PKP is the most commonly performed transplant of choice in ectasia patients. The visual prognosis in PLE cases is excellent, with graft survival rates reported to be 97% at 5 years and 92% at 10 years.⁸ Its complications include graft rejection, induced astigmatism, cataract, increased IOP, endophthalmitis, and retinal detachment.

Deep anterior lamellar keratoplasty (DALK) has recently been advocated for the surgical management of PLE.⁶⁷ It has been performed in PLE cases using both Melles’ manual technique and Anwar's big-bubble technique.^68,69 It effectively restores corneal regularity and improves BCVA. However, high-residual ametropia is often a common finding.

Newer surgical techniques, which have been tried for PLE, include:

Intralamellar keratoplasty (ILK): Schanzlin et al. demonstrated this technique in cases of severe PLE with sagging cones; a donor stromal lenticule is inserted into a stromal pocket of the recipient.⁷⁰
Tuck-in lamellar keratoplasty: Similar to ILK; Jiang et al. used a donor lenticule obtained from patients undergoing SMILE (small incision lenticule extraction) procedure for this technique.⁶²
Flap replacement surgery: Titiyal et al. described this novel procedure in which the LASIK flap is dissected and excised. A donor lenticule with Descemet's membrane and endothelium removed is taken, and tucked into an intrastromal pocket created in the recipient bed, and sutured.⁷¹

PREVENTION

As described above, multiple etiological factors have been described for the development of PLE; however, PLE still often develops in patients who do not have any of these criteria. A review of the published literature incriminates three main culprits, which must be avoided:

Missed ectatic pathologies: These can be prevented by meticulous screening using corneal topography, especially the Belin/Ambrósio display 17on Pentacam® which can predict corneas prone to develop ectasia in the future (Figs. 9A and 9B).
Multiple enhancements: Ectatic disorders must be ruled out before retreatment is considered.
Thinned RSB: RSB must be routinely measured intraoperatively since thickness of flap has been known to vary considerably even in the hands of a single surgeon.

Screening protocols must be in place in every institute where LASIK is done, and it may be individualized based on the surgeon's experience. The Randleman's ectasia score is most commonly used; however, it has been criticized as not being able to detect high-risk patients among those having normal topography.⁷² Various other scoring systems have been developed;⁷³ however, it is essential to develop a customized screening protocol based on the laser machine being used.

Some authors have reported combined procedures which may help to prevent the development of PLE:

Combined LASIK and CXL (LASIK Xtra): CXL serves as a prophylaxis against refractive regression and to prevent the development of PLE in high-risk patients. No associated decrease in visual acuity is seen. Refractive and keratometric outcomes have been shown to be comparable to or better than LASIK alone. No case of PLE has been reported in these patients.^74–78

The following laser refractive procedures have been shown to have lesser risk of development of PLE as compared to LASIK:

Femto-LASIK is more consistent and has more predictable flap size and depth of ablation, and it also causes limited reduction of corneal biomechanical integrity.³⁵
SMILE is thought to preserve the anterior stromal collagen which has a bigger role in the maintenance of corneal integrity.⁷⁹
Photorefractive keratectomy, ASA, and SBK cause lesser reduction in corneal tensile strength compared to LASIK.²⁸

CONCLUSION

Post-LASIK ectasia has not emerged as the epidemic as was predicted by the critics in the early years of refractive surgery. However, even a single case can be problematic considering its medicolegal implications and the number of disability affected life years (DALYs) involved. Hence, every refractive surgeon must be aware of this important complication, and the screening protocols which have been developed for its prevention. It is also equally important to be able to detect its presence early, and provide appropriate management, since early treatment has been shown to have promising visual rehabilitative results. However, despite all screening protocols, ectasia has been seen to develop even in subjects with seemingly no risk factor. Hence, the Joint Consensus Committee of 2005 had recommended that PLE be considered a known risk factor of laser refractive procedures, which may develop despite the strictest screening protocols.18

Figs. 9A and B: Corneal topography of a high-risk patient screened out for laser-assisted in situ keratomileusis. (A) Four maps refractive showing no obvious abnormality apart from high steep K (47.9 D); (B) Belin/Ambrósio display showing suspicious changes in anterior float, predictive of possible future ectasia development.

19The patient should be made aware of this entity before the procedure, and a meticulous follow-up of high-risk patients is essential.

REFERENCES

Kamiya K, Igarashi A, Hayashi K, et al. A multicenter retrospective survey of refractive surgery in 78,248 eyes. J Refract Surg. 2017;33(9):598–602.

Karabela Y, Muftuoglu O, Gulkilik IG, et al. Intraoperative and early postoperative flap-related complications of laser in situ keratomileusis using two types of Moria microkeratomes. Int Ophthalmol. 2014;34(5):1107–14.

Vinciguerra P, Camesasca F, Albè E, et al. Corneal collagen cross-linking for ectasia after excimer laser refractive surgery: 1-year results. J Refract Surg. 2010;26(7):486–97.

Moscovici BK, Campos M. Intrastromal crosslinking in post-LASIK ectasia. Arq Bras Oftalmol. 2014;77(3):191–2.

Seiler T, Koufala K, Richter G. Iatrogenic keratectasia after laser in situ keratomileusis. J Refract Surg. 1998;14(3):312–7.

Tong JY, Viswanathan D, Hodge C, et al. Corneal collagen crosslinking for post-LASIK ectasia: an Australian study. Asia Pac J Ophthalmol. 2017;6(3):228–32.

Pallikaris IG, Kymionis GD, Astyrakakis NI. Corneal ectasia induced by laser in situ keratomileusis. J Cataract Refract Surg. 2001;27(11):1796–802.

Binder PS, Lindstrom RL, Stulting RD, et al. Keratoconus and corneal ectasia after LASIK. J Cataract Refract Surg. 2005;31(11):2035–8.

Randleman JB, Woodward M, Lynn MJ, et al. Risk assessment for ectasia after corneal refractive surgery. Ophthalmology. 2008;115(1):37–50.

Rao SN, Epstein RJ. Early onset keratectasia following laser in situ keratomileusis: case report and literature review. J Refract Surg. 2002;18(2):177–84.

Said A, Hamade IH, Tabbara KF. Late onset corneal ectasia after LASIK surgery. Saudi J Ophthalmol. 2011;25(3):225–30.

Gupta C, Tanaka TS, Elner VM, et al. Acute hydrops with corneal perforation in post-LASIK ectasia. Cornea. 2015;34(1):99–100.

Cheung AY, Heidemann DG. Globe rupture of a post-LASIK keratectasia eye from blunt trauma. Cornea. 2016;35(12):1662–4.

Condon PI. 2005 ESCRS Ridley Medal Lecture: will keratectasia be a major complication for LASIK in the long term? J Cataract Refract Surg. 2006;32(12):2124–32.

Randleman JB, Russell B, Ward MA, et al. Risk factors and prognosis for corneal ectasia after LASIK. Ophthalmology. 2003;110(2):267–75.

Padmanabhan P, Reddi SR, Sivakumar PD. Topographic, tomographic, and aberrometric characteristics of post-LASIK ectasia. Optom Vis Sci. 2016;93(11):1364–70.

Duffey RJ, Leaming D. US trends in refractive surgery: 2004 ISRS/AAO survey. J Refract Surg. 2005;21(6):742–8.

Kerautret J, Colin J, Touboul D, et al. Biomechanical characteristics of the ectatic cornea. J Cataract Refract Surg. 2008;34(3):510–3.

Andreassen TT, Simonsen AH, Oxlund H. Biomechanical properties of keratoconus and normal corneas. Exp Eye Res. 1980;31(4):435–41.

Barraquer JI. Queratomileusis y Queratofakia. Bogota: Instituto Barraquer de America. 1980;405–6.

Amoils SP, Deist MB, Gous P, et al. Iatrogenic keratectasia after laser in situ keratomileusis for less than −4 to −7 diopters of myopia. J Cataract Refract Surg. 2000;26(7):967–77.20

Condon PI, O'Keefe M, Binder PS. Long-term results of laser in situ keratomileusis for high myopia: risk for ectasia. J Cataract Refract Surg. 2007;33(4):583–90.

Santhiago M, Smadja D, Gomes B, et al. Association between the percent tissue altered and post-laser in situ keratomileusis ectasia in eyes with normal preoperative topography. Am J Ophthalmol. 2014;158(1):87–95.

Santhiago M, Smadja D, Wilson S, et al. Role of percent tissue altered on ectasia after LASIK in eyes with suspicious topography. J Refract Surg. 2015;31(4):258–65.

Brenner LF, Alió JL, Vega-Estrada A, et al. Clinical grading of post-LASIK ectasia related to visual limitation and predictive factors for vision loss. J Cataract Refract Surg. 2012;38(10):1817–26.

Huang X, He X, Tan X. [Research of corneal ectasia following laser in situ keratomileusis in rabbits]. Yan Ke Xue Bao. 2002;18(2):119–22.

Tatar MG, Kantarci FA, Yildirim A, et al. Risk factors in post-LASIK corneal ectasia. J Ophthalmol. 2014;2014:204191.

Dawson DG, Grossniklaus HE, McCarey BE, et al. Biomechanical and wound healing characteristics of corneas after excimer laser keratorefractive surgery: is there a difference between advanced surface ablation and sub-Bowman's keratomileusis? J Refract Surg. 2008;24(1):S90–6.

Randleman JB. Post-laser in-situ keratomileusis ectasia: current understanding and future directions. Curr Opin Ophthalmol. 2006;17(4):406–12.

Giri P, Azar DT. Risk profiles of ectasia after keratorefractive surgery. Curr Opin Ophthalmol. 2017;28(4):337–42.

Padmanabhan P, Aiswaryah R, Abinaya PV. Post-LASIK keratectasia triggered by eye rubbing and treated with topography-guided ablation and collagen cross-linking—a case report. Cornea. 2012;31(5):575–80.

Padmanabhan P, Radhakrishnan A, Natarajan R. Pregnancy-triggered iatrogenic (post-laser in situ keratomileusis) corneal ectasia—a case report. Cornea. 2010;29(5):569–72.

Belin M, Ambrόsio R. The Belin/Ambrósio enhanced extasia display. [online] Available from http://aspx.apacrs.org/apacrs-publication/Default2.aspx?id=656.

Binder PS. Analysis of ectasia after laser in situ keratomileusis: risk factors. J Cataract Refract Surg. 2007;33(9):1530–8.

Vahdati A, Seven I, Mysore N, et al. Computational biomechanical analysis of asymmetric ectasia risk in unilateral post-LASIK ectasia. J Refract Surg. 2016;32(12):811–20.

Harissi-Dagher M, Frimmel SA, Melki S. High myopia as a risk factor for post-LASIK ectasia: a case report. Digit J Ophthalmol. 2009;15(1):9–13.

Binder PS. Ectasia after laser in situ keratomileusis. J Cataract Refract Surg. 2003;29(12):2419–29.

Santhiago MR, Giacomin NT, Smadja D, et al. Ectasia risk factors in refractive surgery. Clinical Ophthalmology. 2016;10:713–20.

Dawson DG, Randleman JB, Grossniklaus HE, et al. Corneal ectasia after excimer laser keratorefractive surgery: histopathology, ultrastructure, and pathophysiology. Ophthalmology. 2008;115(12):2181–91.

Ali Javadi M, Kanavi MR, Mahdavi M, et al. Comparison of keratocyte density between keratoconus, post-laser in situ keratomileusis keratectasia, and uncomplicated post-laser in situ keratomileusis cases. A confocal scan study. Cornea. 2009;28(7):774–9.21

Akhtar S, Alkatan H, Kirat O, et al. Ultrastructural and three-dimensional study of post-LASIK ectasia cornea. Microsc Res Tech. 2014;77(1):91–8.

Liu Y, Konstantopoulos A, Riau AK, et al. Repeatability and reproducibility of corneal biometric measurements using the visante omni and a rabbit experimental model of post-surgical corneal ectasia. Transl Vis Sci Technol. 2015;4(2):16.

Maguen E, Maguen B, Regev L, et al. Immunohistochemical evaluation of two corneal buttons with post-LASIK keratectasia. Cornea. 2007;26(8):983–91.

Meghpara B, Nakamura H, Macsai M, et al. Keratectasia after laser in situ keratomileusis: a histopathologic and immunohistochemical study. Arch Ophthalmol. 2008;126(12):1655–63.

Pahuja NK, Shetty R, Deshmukh R, et al. In vivo confocal microscopy and tear cytokine analysis in post-LASIK ectasia. Br J Ophthalmol. 2017;101(12):1604–10.

Elmohamady MN, Abdelghaffar W, Salem TI. Tear martix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in post-LASIK ectasia. Int Ophthalmol. 2018.

Guirao A. Theoretical elastic response of the cornea to refractive surgery: risk factors for keratectasia. J Refract Surg. 2005;21(2):176–85.

Hiatt JA, Wachler BS, Grant C. Reversal of laser in situ keratomileusis induced ectasia with intraocular pressure reduction. J Cataract Refract Surg. 2005;31(8):1652–5.

Kramer EG, Boshnick EL. Scleral lenses in the treatment of post-LASIK ectasia and superficial neovascularization of intrastromal corneal ring segments. Cont Lens Anterior Eye. 2015;38(4):298–303.

Mahadevan R, Jagadeesh D, Rajan R, et al. Unique hard scleral lens post-LASIK ectasia fitting. Optom Vis Sci. 2014;91(4 Suppl 1):S30–3.

Wollensak G, Spoerl E, Seiler T. Riboflavin/ultraviolet-a-induced collagen crosslinking for the treatment of keratoconus. Amer J Ophthalmol. 2003;135(5):620–7.

Greenstein SA, Fry KL, Hersh PS. Corneal topography indices after corneal collagen crosslinking for keratoconus and corneal ectasia: one-year results. J Cataract Refract Surg. 2011;37(7):1282–90.

Poli M, Cornut PL, Balmitgere T, et al. Prospective study of corneal collagen cross-linking efficacy and tolerance in the treatment of keratoconus and corneal ectasia: 3-year results. Cornea. 2013;32(5):583–90.

Kymionis GD, Diakonis VF, Kalyvianaki M, et al. One-year follow-up of corneal confocal microscopy after corneal cross-linking in patients with post laser in situ keratomileusis ectasia and keratoconus. Am J Ophthalmol. 2009;147(5):774–8.

Hersh PS, Greenstein SA, Fry KL. Corneal collagen crosslinking for keratoconus and corneal ectasia: one-year results. J Cataract Refract Surg. 2011;37(1):149–60.

Wan Q, Wang D, Ye H, et al. A review and meta-analysis of corneal cross-linking for post-laser vision correction ectasia. J Curr Ophthalmol. 2017;29(3):145–53.

Wallerstein A, Adiguzel E, Gauvin M, et al. Under-flap stromal bed CXL for early post-LASIK ectasia: a novel treatment technique. Clin Ophthalmol. 2017;11:1–8.

Kanellopoulos AJ, Binder PS. Management of corneal ectasia after LASIK with combined, same-day, topography-guided partial transepithelial PRK and collagen cross-linking: the Athens protocol. J Refract Surg. 2011;27(5):323–31.

Tamayo GE, Castell C, Vargas P, et al. High-resolution wavefront-guided surface ablation with corneal cross-linking in ectatic corneas: a pilot study. Clin Ophthalmol. 2017;11:1777–83.

Zhu W, Han Y, Cui C, et al. Corneal collagen crosslinking combined with phototherapeutic keratectomy and photorefractive keratectomy for corneal ectasia after laser in situ keratomileusis. Ophthalmic Res. 2018;59(3):135–41.22

Carrasquillo KG, Rand J, Talamo JH. Intacs for keratoconus and post-LASIK ectasia: mechanical versus femtosecond laser-assisted channel creation. Cornea. 2007;26(8):956–62.

Jiang Y, Li Y, Yang S, et al. Tuck-in Lamellar keratoplasty with a lenticule obtained by small incision lenticule extraction for treatment of Post-LASIK ectasia. Sci Rep. 2017;7(1):17806.

Tunc Z, Helvacioglu F, Sencan S. Evaluation of intrastromal corneal ring segments for treatment of post-LASIK ectasia patients with a mechanical implantation technique. Indian J Ophthalmol. 2011;59(6):437–43.

Hashemi H, Gholaminejad A, Amanzadeh K, et al. Single-segment and double-segment Intacs for post-LASIK ectasia. Acta Med Iran. 2014;52(9):681–6.

Yildirim A, Uslu H, Kara N, et al. Same-day intrastromal corneal ring segment and collagen cross-linking for ectasia after laser in situ keratomileusis: long-term results. Amer J Ophthalmol. 2014;157(5):1070–6.

Kymionis GD, Bouzoukis DI, Portaliou DM, et al. New INTACS SK implantation in patients with post-laser in situ keratomileusis corneal ectasia. Cornea. 2010;29(2):214–6.

McAllum PJ, Segev F, Herzig S, et al. Deep anterior lamellar keratoplasty for post-LASIK ectasia. Cornea. 2007;26(4):507–11.

Salouti R, Nowroozzadeh MH, Makateb P, et al. Deep anterior lamellar keratoplasty for keratectasia after laser in situ keratomileusis. J Cataract Refract Surg. 2014;40(12):2011–8.

Javadi MA, Feizi S. Deep anterior lamellar keratoplasty using the big-bubble technique for keratectasia after laser in situ keratomileusis. J Cataract Refract Surg. 2010;36(7):1156–60.

Tan BU, Purcell TL, Torres LF, et al. New surgical approaches to the management of keratoconus and post-LASIK ectasia. Trans Am Ophthalmol Soc. 2006;104:212–20.

Titiyal JS, Agarwal T, Jhanji V, et al. Flap replacement surgery for management of post-LASIK ectasia. Br J Ophthalmol. 2010;94(12):1690–2.

Binder PS, Trattler WB. Evaluation of a risk factor scoring system for corneal ectasia after LASIK in eyes with normal topography. J Refract Surg. 2010;26(4):241–50.

Miraftab M, Fotouhi A, Hashemi H, et al. A modified risk assessment scoring system for post laser in situ keratomileusis ectasia in topographically normal patients. J Ophthalmic Vis Res. 2014;9(4):434–8.

Tomita M, Yoshida Y, Yamamoto Y, et al. In vivo confocal laser microscopy of morphologic changes after simultaneous LASIK and accelerated collagen crosslinking for myopia: one-year results. J Cataract Refract Surg. 2014;40(6):981–90.

Nguyen MK, Chuck RS. Corneal collagen cross-linking in the stabilization of PRK, LASIK, thermal keratoplasty, and orthokeratology. Curr Opin Ophthalmol. 2013;24(4):291–5.

Aslanides IM, Mukherjee AN. Adjuvant corneal crosslinking to prevent hyperopic LASIK regression. Clin Ophthalmol. 2013;7:637–41.

Kanellopoulos AJ, Asimellis G. Epithelial remodeling after femtosecond laser-assisted high myopic LASIK: comparison of stand-alone with LASIK combined with prophylactic high-fluence cross-linking. Cornea. 2014;33(5):463–9.

Kymionis GD, Grentzelos MA, Portaliou DM, et al. Corneal collagen cross-linking (CXL) combined with refractive procedures for the treatment of corneal ectatic disorders: CXL plus. J Refract Surg. 2014;30(8):566–76.

Moshirfar M, Albarracin JC, Desautels JD, et al. Ectasia following small-incision lenticule extraction (SMILE): a review of the literature. Clin Ophthalmol. 2017:11:1683-8.

Chapter Notes

Management of Post-LASIK EctasiaCHAPTER 1