Post Lasik Surgery Effects

Patients with post-LASIK infective keratitis tend to present with varying combinations of pain, photophobia, discomfort, redness and discharge. Deterioration in postoperative visual acuity is commonly noted and may be the sole presenting symptom. Patients may also be asymptomatic with the infection identified at a routine postoperative examination. The timing of the onset of symptoms varies – between zero days and several months. This happens due to an error on the part of the eye doctor.

Post-LASIK infections may usefully be divided into early and late groups depending on the length of time from surgery to the onset of symptoms. Those presenting early occur in the first 7–10 days and are more likely to be caused by “typical” Gram-positive bacteria. Late infections, presenting beyond 10 days, are more likely to be atypical infections, especially non-tuberculous mycobacteria but also including fungal infection.

Flap interface infiltrate is the commonest sign evident on examination although infiltrate may be confined to the lamellar flap or the underlying corneal stroma. Other features of infection that may be present are those found in other forms of infective keratitis, including anterior chamber reaction, keratic precipitates, corneal abscess and epithelial defects. Epithelial defects are found far less frequently in post- LASIK keratitis and tend to be associated with Gram-positive infection. The lack of an epithelial defect has important implications for treatment, as topical antimicrobial penetration is poorer in the absence of a defect. An intact epithelium presents a relatively impermeable barrier to topical antibiotic penetration.

TREATMENT

A moistened lint-free sponge may be used to remove residual debris, followed by “soaking” of the flap and stromal bed in antibiotic solution. The choice of antibiotics may depend on whether the keratitis falls into the early or late group. Soaking should be for 2 min or more with each antibiotic solution in turn, followed by careful relaying of the flap. If there is little or no epithelial defect overlying the suspected infection, an epithelial defect should be created to aid antibiotic penetration. Intensive topical antibiotics should then be started (hourly alternating around the clock). The choice of antibiotics will be partly determined by the resistance characteristics of bacteria in the local region. An eye doctor’s advice should be sought if there is doubt.

Topical steroids should be avoided in the early stages of treatment and only instituted, if at all, when there is clear clinical evidence of improvement (e.g. less pain, diminishing and coalescing infiltrate, fewer keratic precipitates, healing epithelial defect), suggesting sterilisation of the offending organism. Introduction of any steroid should generally be in low dose (e.g. twice daily prednisolone sodium phosphate 0.5%) and the response closely monitored for signs of worsening infection, e.g. satellite infiltrates. Steroid use without concomitant antibiotic has been implicated in the recrudescence of infection after apparent sterilisation of Pseudomonas keratitis. Steroid use should be avoided in cases of fungal keratitis.

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