Complications

Each family has its own complications, inherited from its mode of stromal access, plus shared pitfalls. Two scenes concentrate the difficulty: the LASIK interface (several early opacities look alike yet call for opposite treatments) and the PRK surface (epithelial healing → infection, viral reactivation, keratolysis).

8.1 The flap & the cut

At the cut: buttonhole, free or incomplete flap, striae, and later flap displacement after rubbing/trauma. Rarer with femtosecond, these mechanical events still govern final optical quality and set up several interface complications.

8.2 The interface-opacity differential

The core of post-LASIK expertise. Four entities share a cloudy early interface; confusing them risks worsening what you think you are treating.

8.3 Infections

Rare but serious, with a useful chronology: early forms (days) mostly Gram-positive cocci (staph, strep); late forms fearing atypical organisms (non-tuberculous mycobacteria, fungi) at the interface — a sanctuary poorly reached by drops. Do not temporise: lift the flap, sample (smear, cultures, PCR), fortified antibiotics, irrigate the interface. After PRK, infection occurs under the bandage lens.

8.4 Herpetic reactivation

Excimer UV and surgical stress can reactivate latent herpes. In any history of ocular herpes: weigh the indication and, if retained, cover with oral antiviral prophylaxis (aciclovir/valaciclovir) begun before surgery and continued postoperatively.

8.5 NSAID keratolysis

Topical NSAIDs, valuable against early post-PRK pain, can turn toxic and trigger sterile keratolysis (an ulcer that deepens, risking perforation). Risk rises with duration, generics, steroid co-use, and above all a fragile surface (dry eye, neurotrophy, diabetes, systemic disease). Mechanism: matrix proteolysis (MMP/TIMP imbalance). Act without delay: stop the NSAID, intensive lubrication, oral tetracyclines, autologous serum, monitor ulcer depth.

Functional side effects

9.1 Dryness — nerve section & regrowth

The cornea is among the most densely innervated tissues; this innervation drives reflex tear secretion and blink. Every photoablation severs nerves: the circular LASIK flap interrupts the most, surface spares them more, extraction is intermediate. Denervation lowers sensitivity, reduces reflex secretion, slows blink → partly neurotrophic dryness. Regrowth is slow (months to > 1 year), sometimes incomplete — hence possible persistence and a neuropathic surface pain component. Management: substitutes, punctal occlusion, surface anti-inflammatory, and above all time.

9.2 Halos, glare & optical-zone / pupil ratio

Photoablation reshapes only a central disc (optical zone) extended by a transition zone. In photopic conditions the constricted pupil sits within the optical zone → sharp image. In scotopic conditions the dilated pupil overruns the optical zone: peripheral rays cross the transition/untreated cornea, unfocused → halos, glare, ghosting. More marked with a small optical zone, strong correction (abrupt transition) and a large scotopic pupil.

9.3 Presbyopia

Corneal surgery reshapes the cornea but does not restore accommodation: it neither prevents nor treats presbyopia. A subtle point for the myope: previously, myopia gave spontaneous near vision with glasses off; emmetropising removes it, so at the presbyopic age they become dependent on reading glasses — an effect felt as paradoxical if not anticipated. Monovision mitigates the nuisance, at a cost to stereopsis, after selection and a trial.

9.4 Regression & residual error

Over-/under-correction and regression are managed by retreatment when thickness and stability allow; surface haze is now largely prevented by mitomycin C. Iatrogenic ectasia, preventable and serious, is the subject of the next chapter.