December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Lasik Related Stage III Neurotropic Keratitis
Author Affiliations & Notes
  • JC Affeldt
    Ophthalmology Doheny Eye Instit USC School of Newport Beach CA
  • MR Agarwal
    Department of Ophthalmology Ocular Surace Center Doheny Eye Institute Los Angeles CA
  • Footnotes
    Commercial Relationships   J.C. Affeldt, None; M.R. Agarwal, None.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2120. doi:
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    • Get Citation

      JC Affeldt, MR Agarwal; Lasik Related Stage III Neurotropic Keratitis . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2120.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: To describe identification of a multifactorally generated clinical boundary or threshold comprised of corneal sensation and aqueous tear production for development of neurotropic keratitis (NTK). Method: One hundred eyes presenting with all Mackie stages of NTK were evaluated. Initial corneal sensation was quantitated using the Cochet-Bonnet esthesiometer (mean = 6.2mm), while aqueous tear production was documented by Schirmer method with topical anesthesia (mean = 3.1mm). Measurements were statistically compared to values obtained from the unaffected contralateral eye, (mean = 18.6mm and 4.7mm respectively) as well as 32 normal control eyes (mean = 56.3mm and 16.3mm respectively). The data was then graphically analyzed, with sensation and tear production representing the "X’ and "Y’ axis. Results: Irregardless of the underlying etiology, neurotropic keratitis did not become manifest unless their was highly significant loss of both corneal sensation (P=0.0001) and aqueous tear production (P=0.0001) as compared to normals. Not only were both parameters profoundly depressed, but when graphically depicted, they identified a relatively sharp margined boundry line or threshold separating unaffected from diseased eyes. Manipulation of either sensory (topical beta-blockers) or aqueous levels (lacrimal occlusion) could result in threshold crossing, with subsequent disease control. In fact all cases in this series, regardless of presenting clinical stage, were successfully treated by beta-blocker cessation and/or lacrimal occlusion (plug or thermal). Conclusion: An etiologically universal clinical threshold exists, separating normal eyes from manifest neurotropic keratitis. This threshold is created by the co-factored interaction of corneal sensation and aqueous tear production, both of which must be profoundly reduced to produce neurotropic disease. Independent manipulation of either parameter can lead to threshold crossing and disease control. Understanding this threshold concept and its location can provide more accurate diagnosis, as well as more effective therapeutic strategies.

Keywords: 370 cornea: basic science • 449 keratitis • 369 cornea: clinical science 

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