How to Manage Femto LASIK Complications

FS lasers are a benefit to refractive surgery, but come with their own potential complications.

GEORGE O. WARING IV, MD

Since the first femtosecond laser was introduced in 2002, all-laser LASIK using a femtosecond laser has been gaining popularity. Compared to mechanical microkeratomes, the femotosecond laser provides more predictable corneal flap thicknesses, better astigmatic neutrality and decreased risk of epithelial injury.^1,2

The use of femtosecond lasers has become more widespread with the recent release of five new systems: IntraLase FS (Abbot Medical Optics Inc., Santa Ana, CA), Femtec (Technolas Perfect Vision, Heidelberg, Germany), VisuMax femtosecond laser system (Carl Zeiss Meditec, Jena, Germany), Femto LDV (Ziemer Ophthalmic Systems AG, Port, Switzerland) and Wavelight FS200 Femtosecond Laser (Alcon Laboratories Inc., Fort Worth, Texas). In the last few years, femtosecond lasers have become the dominant method of lamellar flap creation. This dominance behooves us to focus on femtosecond laser-related LASIK complications. I’ve outlined them here based on intraoperative and postoperative issues.

Intraoperative Issues

Although rare, occasional surprises can occur during femtosecond laser flap creation. Not uncommonly, this is related to patients’ anatomy. Being familiar with high-risk anatomic features and optimizing head positioning can help minimize potential issues. Most intraoperative challenges are related to suction loss or gas breakthrough.

Suction Loss

The causes of suction loss have been linked to significantly flat keratometric power (K-readings less than 42.00 D), small palpebral apertures, deep-set eyes, excessive eyelid squeezing and a patient’s inability to maintain fixation or follow instructions, or both, among other causes. I previously reported risk factors and management of suction loss related complications.³

The stage of the lamellar cut when the suction loss occurs dictates management of intraoperative suction loss. When suction loss occurs during the raster stage before initiating the side cut, the entire rastermay be repeated with the same diameter and pocket disabled. When suction loss occurs just before starting the side cut or while making it, the raster stage was skipped and the side cut was performed with a smaller diameter. While some clinicians have recommended changing the suction ring, we have found this unnecessary unless the suction was insufficient or the ring was otherwise defective.

You may observe irregular lamellar bed step patterns. In our experience, we have not found these to be visually significant. They may result partly from a smoothing effect from the excimer ablation pattern. Another alternative is to wait one to three months and perform advanced surface ablation.

COURTESY OF UDAY DEVGAN, MD

Figure 1. Intraoperative view of femtosecond laser incisions in cataract surgery made with the Alcon LenSx. Note the presence of small gas bubbles under the anterior lens capsule and the larger, yellow-appearing gas pockets in and around the lens nucleus.

Other Intraoperative Complications

■ Vertical gas breakthrough. This is the femtosecond laser equivalent of a buttonhole from a mechanical microkeratome. FS lasers create a lamellar plane with a plasma separation. Gas breakthrough may occur due to irregular or abnormally thin flaps, corneal pathology or ineffective gas venting. If a full-thickness gas breakthrough occurs, we recommend a healing period of one to three months. I advise serial exams to look for irregular astigmatism and determine a patient’s refractive stability. Once the patient is stable, you can perform surface ablation with mitomycin-C (MMC).

■ Anterior chamber gas bubbles. Gas rarely escapes into the anterior chamber, but it can cause issues when it does (Figure 1). Some researchers have speculated that air can occasionally track through Schlemm’s canal into the anterior chamber. I have previously reported that anterior chamber air bubbles resulting from a femtosecond laser do not affect endothelial cell density when compared to normal eyes in a large series.⁴ The bubbles can affect tracking in certain lasers, and you can either dilate and track while the pupil is enlarging, or wait for the bubbles to resorb.

Postoperative Complications

Although postoperative complications can arise any time, typically most manifest within the first few months postoperatively. Postoperative femto-LASIK complications can be organized into flap, interface or biomechanical issues.

Flap Dislocation

Flap dislocation typically presents within the first 24 hours postoperatively, unless it is traumatic. Patients will experience an immediate decrease in visual acuity and significant pain. This is often related to mechanical trauma such as inadvertent eye rubbing and, on occasion, dryness with inadequate lubrication.

We recommend lubrication, frequent eye blinking and use of protective glasses or shields in the early postoperative period. Treat any appreciable flap dislocation as an emergency. Immediately refloat the flap and reposition it after inspecting and cleaning the lamellar interface. Pay careful attention to removing the epithelial tags at the flap edge. You can place a bandage contact lens once you’ve repositioned the lamellar flap.

Treat late traumatic flap dislocation in the same manner, unless the flap has been lacerated. If possible, attempt reapproximation. If the flap has been severely damaged, amputate it at the hinge with surgical scissors, then place a bandage contact lens until the stromal surface reepitheliazes. After the patient achieves refractive stability, usually after three to six months, you can perform surface ablation with MMC for residual refractive error. The patient should understand the possibility exists of needing a rigid contact lens for residual irregular refractive error.

Flap Striae

Although flap striae are really intraoperative complications, they often go unnoticed until after surgery. You can avoid them by carefully examining the flap immediately at the conclusion of the procedure. Applying a few seconds of compressed oxygen to the corneal surface not only helps the flap seat better and it reveals striae or Bowman’s “crinkles” (microstriae). Evaluate the gutter symmetry by aspirating gutter fluid with a weck cell or using a vitrectomy light pipe tangentially.

At the biomicroscope, retroillumination is the most effective way to evaluate striae. Peripheral macrostriae and often central Bowman’s crinkles do not typically result in symptoms. You may monitor them. If the patient is symptomatic with central macrostriae, immediately re-float the flap, then gently stretch it to relieve striae with weck cells. Longstanding, clinically significant striae may require epithelial debridement before stretching.

Diffuse Lamellar Keratitis

A diffuse white, granular infiltrate that typically manifests within a few postoperative days characterizes this sterile inflammation of the lamellar interface. The etiology of DLK is still unknown, but it seems to have multiple causes, among them povidone-iodine solutions, hemoglobin, carboxymethylcellulose drops, bacterial endotoxins, surgery-related epithelial defects, microkeratome blade debris, atopy, marking pens, toxic chemicals, meibomian secretions, traumatic flap dislocation or subsequent surgical repair.^5-7

Symptoms of DLK include blurred vision and photophobia, although many patients do not experience any symptoms in the early stages (Figure 2, page 54). The stages of DLK are:

► Stage I — white granular cells in the laminar flap periphery outside the visual axis. It is not uncommon.

► Stage II — white granular cells in the center of the laminar flap involving the visual axis. This is more frequently seen on two or three days postoperatively, and results from the central migration of cells in stage I.

► Stage III — an aggregation of more dense white clumped cells in the central visual axis, often associated with decreased visual acuity.

► Stage IV — a rare finding that results from severe laminar keratitis and stromal melting. It can cause permanent scarring and hyperopic shift. Aggregation of inflammatory cells and the release of collagenase, resulting in fluid collection with overlying bullae formation and stromal melting, characterize Stage IV. Robert Maloney, MD, was the first to suggest that central toxic keratopathy and stage IV DLK were separate entities.⁸

Once you recognize the symptoms of DLK, you must treat it immediately to prevent its progression. Worsening cases may lead to scarring, stromal melt, haze, hyperopic shift, irregular astigmatism or permanent visual loss. DLK is usually self-limiting or treated with topical steroids in its early stages.

Severe cases require, flap lifting, BSS irrigation and steroid therapy. We have had success treating stage IV with in-office hyperosmotic application (topical glycerol) and outpatient topical hyperosmotic agents, suggesting that edema plays a large part in the refractive changes and likely underlying pathology.

Epithelial Ingrowth

Intraoperative disturbance of the corneal epithelium seems to be the underlying cause of epithelial ingrowth. Poor flap adhesion may allow epithelial cells to grow into the flap interface. Epithelial ingrowth is usually asymptomatic. It is diagnosed during slit-lamp examination or with high-resolution imaging such as Schiempflug imaging high fourier domain OCT, usually within three months postoperatively. Decreased vision may occur secondary to astigmatic changes from irregular flap contours as the underlying cells cause focal areas of topographic elevation.

Less commonly, the astigmatic changes stem from cell migration into the visual axis. Occasionally patients will complain of dryness or foreign-body sensation and light sensitivity. In advanced cases, flap melting secondary to collagenase release from hypoxic epithelial cells underneath the flap can occur.

Pay attention to minimal epithelial manipulation and accurate flap apposition. Be especially careful to remove any epithelial tags from the interface at the flap edge and reapproximate the flap with the area peripheral to the flap edge. If an intraoperative epithelial defect manifests, strongly consider a bandage contact lens. When performing enhancement, it’s critical that you give attention to removing the peripheral epithelium from the flap interface and obtaining excellent flap apposition when replacing the flap.

COURTESY: GITANE PATEL, MD, M.P.H. AND JAY S. PEPOSE, MD, PH.D.

Figure 2. A patient one day following LASIK presented with pain, decreased vision and focal clustered infiltrates, some extending beyond the flap margin. These are warning signs of early LASIK-associated microbial keratitis, requiring flap lift, culture and scraping, antibiotic irrigation of the interface and intensive antibiotic treatment.

Patients with grade 1 epithelial ingrowth should be seen weekly for one month. Accurate documentation and measurements will help determine stability or progression. When epithelial ingrowth stabilizes, resume routine follow-up care. For primary treatments, I simply lift the flap and scrape the epithelial cells from the stromal bed and under-surface of the flap. Typically, I follow this by placing a bandage contact lens.

The recurrence rate of lifting and scraping the cells alone has been reported to be as high as 44%.^9-12 For these recurrent episodes, I suture the flap in the sector of ingrowth after removing the epithelial cells to improve apposition between the flap and the stromal bed. Place the suture with enough space from the flap edge to avoid disturbing the epithelium with suture removal.

For recalcitrant cases, I will suture the entire flap after repeating debridement. Adjunctive gluing of the flap after epithelial debridement to improve flap adhesion to the stromal bed has also had favorable outcomes. Nd:YAG laser is another method used to destroy epithelial cells. For advanced or recalcitrant cases with flap melting, consider flap amputation.

Infectious Keratitis

Cases of post-LASIK infectious keratitis generally fall into two groups: early and late onset. In early onset infectious keratitis, gram-positive cocci, such as staphylococci and streptococci, are the most likely culprits. Late-onset infectious keratitis is more due to opportunistic microbes such as atypical mycobacteria, Nocardia and fungi. Once you confirm the diagnosis, I recommend lifting the flap and preforming gram stain and culture of the interface foci for guidance on antibiotic therapy.

Initial treatment includes lifting the flap and irrigating the interface with appropriate antibiotics, again guided by the time of onset. Then start the patient on frequent topical antibiotic therapy and observe closely. Tailor antibiotic therapy to the gram stain and culture findings.

Ectasia

A history of progressive myopia and astigmatism after refractive surgery coupled with clinical and topographic findings consistent with ectasia are suggestive of a diagnosis of post-LASIK ectasia. Topographic findings of post-LASIK ectasia mimic the non-iatrogenic variety, although extreme keratometric steepening may be absent due to the intentional corneal flattening of LASIK for myopia. Be careful not to misdiagnose prior hyperopic LASIK as ectasia, although this can occur.

Post-LASIK ectasia can progress rapidly, and we recommend immediate corneal collagen crosslinking once diagnosed.

Intacs (Addition Technology, Inc., Des Planes, Ill.) are another option. These are quite useful for improving the refractive component of ectasia and helping patients get back into a contact lens. For advanced cases, we recommend deep anterior lamellar keratoplasty (DALK).

GP and hybrid contact lenses may be indicated in these patients. Advances in combined therapies are on the horizon. They involve combining crosslinking with LASIK to minimize the risk of ectasia after LASIK, as well as topography-guided limited surface ablation combined with crosslinking for both biomechanical and optical therapy.

Other Postoperative Complications

■ Postoperative haze. Originally described by Krishna Rocha and other investigators at Cole Eye Institute of the Cleveland Clinic, you may observe postoperative haze, similar to haze after surface ablation, with ultra-thin flap LASIK.¹³ Researchers believe the mechanism is similar to cytokine-activated fibroblastic activity in ultra-thin flaps (90 μm or less). Typically, these cases are mild, although refractive changes can occur. Topical steroids are indicated.

■ Transient light sensitivity syndrome. Acute onset of photophobia after femto LASIK without changes in acuity or other clinical findings characterizes TLSS. It typically manifests between two to six weeks postoperatively. Fluorescent lights often exacerbate symptoms. TLSS was more common with the early generation femtosecond lasers, likely because they delivered more energy to the cornea with lower repetition rates. TLSS is not sight-threatening and is easily to treat with a topical low-dose steroid taper.

Bottom Line: Be Prepared

LASIK has an excellent safety and efficacy record, being one of the most common and well-established elective surgical procedures offered worldwide. Never has the technology of both femtosecond and excimer lasers been more advanced. But as with all surgical procedures, complications can occur. We need to be familiar with techniques in diagnosis and management. OM

References

1. Kato N, Toda I, Hori-Komai Y, Sakai C, Tsubota K. Five-Year Outcome of LASIK for Myopia. Ophthalmology. 2008;115:839-844.

2. Asano-Kato N, Toda I, Hori-Komai Y, Takano Y, Tsubota K. Risk Factors for Insufficient Fixation of Microkeratome During Laser in situ Keratomileusis. J Refract Surg. 2002;18:47-50.

3. Tomita M, Watabe M, Nakamura T, Nakamura N, Tsuru T, Waring GO 4th. Management and outcomes of suction loss during LASIK flap creation with a femtosecond laser. J Refract Surg. 20122;8:32-6.

4. Tomita M, Watabe M, Waring GO 4th, Durrie DS. Corneal endothelial cell density after myopic intra-LASIK and the effect of AC gas bubbles on the corneal endothelium. Eur J Ophthalmol. 2011;21:363-7.

5. Smith RJ, Maloney RK. Diffuse lamellar keratitis; a new syndrome in lamellar refractive surgery. Ophthalmology 1998;105:1721-1726

6. Linebarger EJ, Hardten DR, Lindstrom RL: Diffuse lamellar keratitis: diagnosis and management. J Cataract Refract Surg. 2000;26:1072-1077.

7. Linebarger EJ, Hardten DR, Lindstrom RL: Diffuse lamellar keratitis: identification and management. Int Ophthalmol Clin. 2000;40:77-86.

8. Sonmez B, Maloney RK. Central toxic keratopathy: description of a syndrome in laser refractive surgery. Am J Ophthalmol. 2007;143:420-427.

9. Wang MY, Maloney RK. Epithelial ingrowth after laser in situ keratomileusis. Am J Ophthalmol. 2000 Jun;129:746-51.2.

10. Asano-Kato N, Toda I, Hori-Komai Y, et al. Epithelial ingrowth after laser in situ keratomileusis: clinical features and possible mechanisms. Am J Ophthalmol. 2002;134:801-807.

11. Kamburoglu G, Ertan A. Epithelial ingrowth after femtosecond laser-assisted in situ keratomileusis. Cornea. 2008;27:1122-1125.

12. Letko E, Price MO, Price FW Jr. Influence of original flap creation method on incidence of epithelial ingrowth after LASIK retreatment. J Refract Surg. 2009;25:1039-1041

13. Rocha KM, Kagan R, Smith SD, Krueger RR. Thresholds for interface haze formation after thin-flap femtosecond laser in situ keratomileusis for myopia. Am J Ophthalmol. 2009;147:966-972, 972.e1. doi: 10.1016/j.ajo.2009.01.010. Epub 2009 Mar 27

George O. Waring IV, MD, is director of refractive surgery and assistant professor at Storm Eye Institute, Medical University of South Carolina, Charleston. He also serves as an adjunct assistant professor of bioengineering at Clemson University in South Carolina. Dr. Waring is a consultant and medical advisory board member for technologies mentioned.