LASIK Complications

From EyeWiki


LASIK complications can be categorized to intraoperative and postoperative complications:

Intraoperative Complications

The intraoperative complication rate has been reported between 0.7-6.6%[1], most commonly microkeratome-related, either mechanical or femtosecond (FS) Laser.

Microkeratome-related flap complications

Flap Buttonhole

caused by buckling of the cornea during flap creation, occurs predominantly in steep corneas. Other risk factors include loss of suction, defective blade, abnormal advancement of blade.

Management: Do not perform laser ablation, recut the flap and ablate a minimum of 3 months later.[1]

Free Cap

caused by inadequacy of captured tissue in the suction ring, occurs predominantly in flat cornea. To prevent free cap, use larger ring and choose larger flap hinge.

Management: Perform laser ablation, orient the cap properly and replace it on the bed, allow air-drying for 3-5 minutes.[1]

Incomplete, short, or irregular flaps

caused by inadequate suction or microkeratome malfunction.

Management: Do not manipulate the flap, do not perform laser ablation, place a bandage contact lens, and recut the flap and ablate at least 3 months later.[1]

Corneal perforation

is a rare but devastating complication. It has been reported in older model of mechanical microkeratomes when it was not properly assembled or the depth plate was not properly placed. [2][3] It can also occur during laser ablation on extremely thin cornea.[4][5]

Management: Immediately de-activate the suction, remove the microkeratome, and repair the perforation in sterile manner.[1]

Vertical gas breakthrough

occurs during FS laser-assissted flap creation, resulting in escape of gas bubbles from the dissection plane into the subepithelial space. The cause is unknown but a thin flap or a focal break in the Bowman's layer may consider.[6]

Management: Lift the flap cautiously and perform laser ablation.[6]

Anterior chamber gas bubbles

occurs during FS laser-assissted flap creation, resulting in escape of gas bubbles from the dissection plane into the trabecular meshwork then to the anterior chamber.[7] The anterior chamber bubbles can interfere with pupillary tracking, but usually are self limiting and resolve over a short period of time.[8][9]

Corneal Epithelial Defect

The risk factors of epithelial erosion during LASIK include older age, previous corneal trauma, diabetes mellitus, epithelial basement membrane dystrophy (EBMD), and type of microkeratome. It can also occur in FS laser microkeratome with a reduced incidence. Epithelial defect can predispose to delayed healing, diffuse lamellar keratitis (DLK), epithelial ingrowth, flap striae, and infectious keratitis.

Prevention: limiting toxic topical medications, minimizing use of topical anesthetics, frequent use of lubricating drops, preoperative inspection of blade and meticulous microkeratome maintenance.

Management: Use bandage soft contact lens for larger defect (>1 mm), topical lubricants until re-epithelialization establishes.[10]

Limbal Bleeding

It occurs in two occasions: presence of corneal pannus as is common in contact lens wearers, using inappropriate size or position of the suction ring resulting in passage of the blade over limbal or conjunctival vessels.

Management: Apply gentle pressure on the oozing vessels with a dry sponge directly or pushing a fold of conjunctiva over the limbal feeders with a dry sponge. Remove any blood in the ablation zone. After replacing the flap, phenylephrine 2.5% may be used to constrict the blood vessels.[1]

Interface Debris

The sources include meibomian gland secretions, particles from sponge, talk from gloves, metallic fragment from blade, red blood cells, epithelial cells, and debris from tear film. [11]

Prevention: Use an aspirating speculum, operate in a lint-free environment, drape the lashes and eyelids.

Management: Only if an inflammatory reaction elicited by debris, then lift the flap, irrigate and remove the debris manually. Otherwise they are well tolerated.[10]

Postoperative Complications

Overcorrection and Undercorrection

Undercorrection is the most common complication after primary LASIK. Overcorrection is mostly seen after retreatment.[12] Both are related to the ablation algorithm, nomogram, age, and the amount of refractive error.[13][14]

Flap Fold or Striae

The risk factors for flap folds include excessive irrigation of flap during LASIK, poor repositioning of the flap at the end of procedure, thin flaps, deep and highly myopic ablation with flap-bed mismatch. Flap folds may be classified into macro- and microstriae.

Macrostriae

Macrostriae are full thickness, rolling stromal folds, occur because of flap malposition or slippage.

Management: Perform immediate refloating and repositioning. After 24 hours, need refloating, de-epithelialization, hydration, stroking, and suturing.[10]

Microstriae

Microstriae are fine folds in Bowman’s layer, occur because of mismatch of flap to new bed and often visually insignificant.

Management: Observation with aggressive lubrication, if visually significant perform refloating, stroking, and suturing.[10]

Flap Dislocation

The risk factors are excessive lid squeezing, eye rubbing, excessive dry eye, presence of epithelial abrasion, poor intraoperative repositioning, excessive irrigation of flap, and trauma.

Prevention: Check adhesion of flap at the end of procedure, Remind the patient not to squeeze or rub the eyes and wear the shield for the first 24 hours and every night for the first week.

Management: Reposition the flap, Suture the flap in the event of persistent fold, and use lubricants.[1]

Dry Eye and Corneal Sensation

Dry eye is one of the most common side effects of LASIK in 60-70% of all patients with varying degrees due to corneal denervation.

Prevention: Perform a thorough exam preoperatively to discover dry eye syndrome and treat aggressively with topical lubrication, cyclosporine A, and systemic treatment with oral tetracyclines, and oral omega-3 fatty acids.

Management: mild dry eye syndrome: frequent use of non-preserved artificial tears, and gels.Severe dry eye syndrome: topical cyclosporine A, topical corticosteroid, oral tetracyclines, oral omega-3 fatty acids, and punctual occlusion. [10]

Diffuse Lamellar Keratitis (DLK)

See the discussion in Diffuse Lamellar Keratitis section.

Pressure-induced Stromal Keratitis (PISK)

PISK is a late-onset interface opacity similar to DLK with a visible fluid cleft in the interface as a result of elevated IOP because of prolonged corticosteroid treatment.

Management: rapid tapering or cessation of the corticosteroids and use of anti-glaucoma medication to lower IOP. [10]

Central Toxic Keratitis (CTK)

See the discussion in Central Toxic Keratitis section.

Infectious Kertatitis

Infection under a LASIK flap is one of the most vision threatening complications. The most common organisms are gram-positive bacteria followed by atypical mycobacteria.

Symptoms: decreased vision, pain, photophobia, and redness

Differential Diagnosis: DLK that usually seen within first 24 hours and typically begins at flap periphery

Prevention: Adequate sterilization of the instruments, preoperative treatment of blepharitis, use of sterile surgical technique, postoperative antibiotic prophylaxis.

Management: Lift the flap, culture the interface, and irrigate with antibiotics. Start empirical fortified treatment including vancomycin (50 mg/ml), tobramycin (14 mg/ml), or gatifloxacin, moxifloxacin.

Atypical mycobacteria: topical clarithromycin (10 mg/ml), oral clarithromycin (500 mg bid), and topical amikacin (8 mg/ml)Fungal keratitis: Natamycin (50 mg/ml), amphotricin (1.5 mg/ml).[10]

Epithelial Ingrowth

The risk factors are poor adhesion of the flap edges, epithelial abrasions at the flap margin, buttonhole flap, free cap, ablation at the edge of stromal bed, epithelial irregularity at the edge of flap, introduction of epithelial cells during the cut, or insertion of instruments, inadequate irrigation, previous RK, reoperation.

Two types of epithelial ingrowth recognized: isolated epithelial pearls in the interface, and epithelial sheet growing into the interface from the periphery.[1]

Symptoms: reduced vision, irregular astigmatism, and risk of stromal melting.

Prevention: Avoid epithelial abrasion, remove epithelial cells and debris from the interface, and avoid wide ablation zone.

Management: No treatment for asymptomatic isolated nests, otherwise lift the flap and scrape both the underside and the stromal bed then reposition the flap.[10]

Ectasia

See the discussion in Post Lasik Ectasia section.

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Azar DT, Koch DD. LASIK: Fundamentals, surgical techniques, and complications. New York. Basel, Marcel Dekker, Inc. 2003
  2. Brint SF, Ostrick M, Fisher C, et al. Six-month results of the multicenter phase 1 study of excimer laser myopia keratomileusis. J Cataract Refract Surg 1994;20:610-615.
  3. Pallikaris IG, Siganos DS. Excimer laser in situ keratomileusis and photorefractive keratectomy for correction of high myopia. J refract Corneal surg 1994;10:498-510
  4. Joo CK, Kim TG. Corneal perforation during laser in situ keratomileusis. J Cataract Refract Surg 1999;25:1165-1167
  5. Mulhern MG, Condon PI, O’Keefe M. Endophthalmitis after laser in situ keratomileusis. J Cataract Refract Surg 1997;23:948-950.
  6. 6.0 6.1 Srinivasan S, Herzig S. Sub-epithelial gas breakthrough during femtosecond laser flap creation for LASIK. Br J Ophthalmol 2007; 91:1373
  7. Soong HK, Malta JB. Femtosecond lasers in Ophthalmology. Am J Ophthalmol 2009; 147:189-197
  8. Srinivasan S, Rootman DS. Anterior chamber gas bubble formation during femtosecond laser flap creation for LASIK. J Refract Surg 2007; 23:828-830
  9. Lifshitz T, Levy J, Klemperer I, Levinger S. Anterior chamber gas bubbles after corneal flap creation with a femtosecond laser. J Cataract Refract Surg 2005; 31:2227-2229
  10. 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 Rapuano CJ, Belin MW, Boxer-Wachler BS, et al. Refractive surgery. Basic and Clinical Science Course, Section 13. San Francisco CA. AAO 2009-2010.
  11. Hirst LW, Vandeleur KW. Laser in situ keratomileusis interface deposits. J refract Surg 1998;14:653-654
  12. Ozdamar A, Sener B, Aras C, Aktunc R. Laser in situ keratomileusis after photorefractive keratectomy for myopic regression. J Cataract Refract Surg 1998; 24:1208-1211.
  13. Huang D, Stulting RD, Carr JD, Thompson KP, Waring III GO. Multiple regression and vector analysis of Laser in situ keratomileusis for myopia and astigmatism. J refract Surg 1999;15:538-549.
  14. Ditzen K, Handzel A, Pieger S. Laser in situ keratomileusis nomogram development. J refract Surg 1999;15(suppl):S197-S201.