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Keratectasia after PTK
  1. Simon J Dean,
  2. Charles N J McGhee
  1. Discipline of Ophthalmology, Faculty of Medicine and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand
  1. Correspondence to: Professor C N J McGhee; c.mcghee{at}auckland.ac.nz

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Takahashi and colleagues have elegantly described an interesting and rare complication of phototherapeutic keratectomy (PTK) in their recent report of an unusual case of keratectasia after PTK.1 The hypothesis that risk of ectasia is proportional to residual stromal base, or depth of ablation, fits with the assumed biomechanical aetiology of this recently reported complication of laser refractive surgery. The generally accepted empirical minimum thickness of 250–300 μm of corneal stroma, excluding flap thickness, remains speculative, as we do not understand the underlying pathophysiology. Indeed, although Holland et al highlighted the association of thin residual stromal thicknesses, post-PRK and LASIK, with keratectasia, they also described this complication after surface based hypermetropic PRK ablation, where the centre was minimally ablated and residual stromal thickness was greater than 360 μm.2

The authors suggest, in the reported case, that band-shaped keratopathy (BSK) may have compromised the tensile strength of the cornea. This seems unlikely as this condition generally affects the superficial anterior cornea, and usually does not penetrate deeper than Bowman's layer, hence its suitability for treatment by PTK. However, further clinical detail which the authors have not provided might reveal underlying corneal pathology with secondary “rough” BSK rather than “smooth” BSK.

However, there are a number of reasons, other than simple biomechanical compromise, for keratectasia following PTK in this case: (1) forme fruste keratoconus—as no preoperative topography or surface asymmetry values are presented to enable the reader to rule this out; (2) clinical keratoconus, which seems less likely in respect of patient's age and a preoperative cylindrical error of only −1.5D; (3) idiopathic keratectasia, possibly secondary to widespread deregulated keratocyte apoptosis. The latter has been demonstrated after LASIK, with a considerable and longstanding decrease in keratocytes in the peri-ablation area.3 Also, Helena et al4 demonstrated apoptosis to a depth of at least 50 μm after all of the following procedures: epithelial scrape, corneal scrape PRK, transepithelial PRK, and LASIK. Epithelial scrape and LASIK demonstrated keratocyte apoptosis to depths of up to 75 μm and 100 μm, respectively. The authors have recently identified a keratocyte free zone 160 μm into the stroma following LASIK, and theoretically more widespread apoptosis as a response to excimer laser photorefractive surgery, may contribute to keratectasia.

While it is difficult to ascertain why keratectasia occurs, in this case with a residual stromal thickness of over 500 μm, from the data provided the most likely aetiologies would seem to be either undiagnosed forme fruste keratoconus or idiopathic keratectasia. Currently,5 recent reviews illustrate the dearth of substantial information available regarding idiopathic keratectasia (iatrogenic keratoconus), with a little over 60 cases published. At this point, although some are likely to be due to over-ablation, for many cases such as this the exact aetiology remains unknown and is likely to be multifactorial, and one of these factors is residual corneal thickness. The fact that keratectasia can occur, after what would be considered minimal ablation, highlights the unpredictability of occurrence, but with over a million cases of LASIK or PRK occurring each year, the stimulus to identify contributing factors is significant.

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