Jl. Alio et al., Postoperative inflammation, microbial complications, and wound healing following laser in situ keratomileusis, J REFRACT S, 16(5), 2000, pp. 523-538
Although the biology of corneal wound healing is only partly understood, he
aling after photorefractive keratectomy (PRK) and laser in situ keratomileu
sis (LASIK) differs in many respects, and the mechanisms appear to be diffe
rently controlled. There is less of an inflammatory and healing response af
ter LASIK, but a longer period of sensory denervation. The cellular, molecu
lar, and neural regulatory phenomena associated with postoperative inflamma
tion and wound healing are likely to be involved in the adverse effects aft
er LASIK, such as flap melt, epithelial ingrowth, and regression, Interface
opacities in the early postoperative period include diffuse lamellar kerat
itis (DLK), microbial keratitis, epithelial cells, and interface opacities.
Diffuse lamellar keratitis (sands of the Sahara syndrome) describes an app
arently noninfectious diffuse interface inflammation after lamellar corneal
surgery probably caused by an. allergic or a toxic inflammatory reaction.
Noninfectious keratitis must be distinguished from microbial keratitis to a
void aggressive management and treatment with antimicrobial drugs. Microbia
l keratitis is a serious complication after LASIK, but a good visual outcom
e can be achieved following prompt and appropriate treatment.