OcuLearning › Cornea
Corneal Refractive Surgery Complications
URGENT — Cornea
Symptoms
Early (1–14 days)
- Decreasing visual acuity.
- Increased pain.
Late (2 weeks – several months)
- Decreasing visual acuity.
- Severe glare and monocular diplopia.
- Dry-eye symptoms (burning, foreign body sensation).
Clinical Findings
DLK (sands of the Sahara)
- Fine granular white cells in the LASIK flap interface (typically days 1–5).
- Sterile, non-infectious; lacks epithelial defects or significant conjunctival injection.
- Stages 3–4: central confluent cells with vision loss; requires flap lift and irrigation.
Epithelial ingrowth
- Pearly gray-white nests or fronds under the flap edge.
- May cause flap edge elevation, irregular astigmatism, or stromal melt.
Post-LASIK ectasia
- Progressive inferior corneal steepening and thinning.
- Results in increasing irregular astigmatism.
PISK (pressure-induced stromal keratitis)
- Interface fluid resulting from steroid-induced intraocular pressure (IOP) rise.
- Mimics DLK appearance.
- Critical check: central IOP readings are falsely low; must measure IOP peripheral to the flap edge.
Flap complications
- Dislocation: usually occurs within the first 24 hours.
- Striae/Microstriae: fine folds in the flap that may be visually significant.
- Buttonholes or free caps (incomplete or detached flaps).
Post-PRK findings
- Corneal haze: subepithelial scarring (prevented by intraoperative Mitomycin-C).
- Delayed epithelial healing or refractive regression.
Ocular surface
- Dry eye/neurotrophic keratopathy: most common complication due to transected corneal nerves.
Etiology
Inflammatory & immune
- DLK: sterile response to interface contaminants (debris, meibum, endotoxins, glove powder).
- PISK: transudation of aqueous into the interface due to steroid-induced OHT.
- Corneal haze: aggressive wound healing response following PRK.
Mechanical & anatomical
- Epithelial Ingrowth: displacement of cells during surgery or migration through poor edge apposition.
- Ectasia: excessive stromal ablation (residual bed <250–300 μm) or unrecognized preoperative keratoconus.
- Dry Eye: disruption of the homeostatic reflex due to corneal nerve transection.
Red Flags
Post-LASIK ectasia (progressive thinning) → must perform cross-linking; no further ablation.
Flap dislocation or significant striae → urgent surgical repositioning required.
Stage 3–4 DLK → requires immediate aggressive steroids and interface irrigation.
Interface infection → mandates flap lift for culture; must cover atypical mycobacteria and fungi.
Investigations
Clinical exam
- Slit-lamp evaluation with fluorescein to assess the flap interface and epithelium.
- Refraction: perform hard contact lens overrefraction to identify irregular astigmatism.
Tonometry
- Use Tono-Pen/Applanation; measure peripherally if PISK is suspected.
Imaging
- Corneal topography/tomography (e.g., Pentacam) to evaluate for ectasia or irregular astigmatism.
- Schirmer testing for severe dry eye symptoms.
Treatment
DLK management
- Intensive Prednisolone acetate 1% every hour.
- Severe cases: lift flap and irrigate the interface to remove inflammatory cells.
PISK management
- Discontinue topical steroids rapidly.
- Initiate ocular hypotensive (IOP-lowering) medications.
Epithelial ingrowth
- Observation for peripheral, non-progressive cases.
- Surgical debridement/scrape for progressive or vision-threatening growth.
Ectasia & haze
- Ectasia: corneal cross-linking (CXL); visual rehab with scleral lenses.
- PRK Haze: increase steroid frequency; consider PTK with Mitomycin-C for severe cases.
Flap repair
- Dislocation/Striae: lift, irrigate, and refloat the flap.
- Lost flap: manage as a large epithelial defect.
Clinical Pearl
Post-LASIK ectasia mimics keratoconus on topography; the treatment is early cross-linking and specialty contact lenses, never more laser ablation.
Differential Diagnosis
- Dry eye disease
- Natural refractive regression
- Epithelial ingrowth
- Corneal ectasia
- Infectious keratitis