Post on 30-Jan-2016
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Biomechanics of Hyperopic Shift in Stage 4 Diffuse Lamellar Keratitis
and Central Toxic Keratopathy
Brian R Will, MDAdjunct Clinical Professor of OphthalmologyLoma Linda University School of Medicine
Loma Linda, California
Medical DirectorWill Vision and Laser Centers
Vancouver, Washington
No Financial Interest
Brian R Will, MDAdjunct Clinical Professor of OphthalmologyLoma Linda University School of Medicine
Loma Linda, California
Medical DirectorWill Vision and Laser Centers
Vancouver, Washington
No Financial Interest
Patient Series8 eyes with Stage 4 DLK All eyes studied using time matched
Pentacam imaging Tangential Power Map Elevation Map Scheimphlug photographic images
Optical Coherence Tomography Hi Resolution Corneal images
Imaging began at presentation of Stage 4 DLK
All eyes ultimately recovered 20/20 BSCVA
Central flatteningMid peripheral steepeningPeripheral flattening
Day 1 to 5
Central steepeningMid peripheral flatteningPeripheral steepening
Day 12 to 112
ReversalTangential
Power
Map
Analysis
Flap initially thin - Day 1 of Stage 4 DLK Residual Stromal Bed normal - Day 1
Flap markedly thickens by Day 12 Residual Stromal Bed marked thinning
Flap resumes normal thickness over time Residual Stromal Bed normal over time
Flap initially normal thickness
Thickens by 40 microns or more
Then becomes normal over time
Residual stromal bed normal
Thins by 50 microns or more
Then becomes normal over time
With injury / epithelial cell removal Anterior cornea swells Posterior cornea thins
Caused by changes in interstitial fluid pressure Change induced by inflammatory cytokines
Did not study the reversibility of the phenomenon Failed to recognize the biomechanical impact of these fluid shifts Incorrectly identified keratocyte apoptosis as the
mechanism for changes in Pif
Key Concepts - Biomechanics of the Hyperopic Shift Induced by effects of inflammatory
cytokines on interstitial fluid pressures (Pif)
Corneal shape is controlled by the complex relationship between Localized changes in Pif Localized changes in tissue tension Localized changes in tissue compliance
Flap edema created by compliance mismatch between flap and RSB
Local Control of Corneal Pif Complex interaction between keratocytes and ECM
modulated by Inflammatory cytokines Transmembrane proteins - Integrins Actin cell cytoskeleton Outside-In transmembrane signaling
Pif is Not uniform in the cornea Central cornea 5X more negative
than limbus Endothelial function cannot
create this gradient
Pif gradient drives fluid from periphery to center
Relationship between Pif and Tissue tension
Tissue compliance determines the volume of fluid (∆Vol) a tissue can hold at a given Pif (∆Pif)
Compliance is affected by tissue tension Higher tension - less compliant Lower tension - more compliant
∆ Pif
∆ Tissue Volume
Normal ComplianceNormal Thickness
LASIK FlapIncreased ComplianceTissue thickens
Residual Stromal BedDecreased ComplianceTissue thins
Biomechanical Dynamic
Inflammatory cytokines
Inflammatory cytokines
Inflammatory cytokines drive Pif negative
Flap has low tension and high compliance
Flap imbibes fluid, swells and thickens
Inflammatory cytokines drive Pif negative
Lowered Pif pulls fluid from the limbus
Mid peripheral cornea imbibes fluid, swells
and thickens
Inflammatory cytokines drive Pif negative
Lowered Pif pulls fluid from the limbus
Mid peripheral cornea imbibes fluid, swells
and thickens
As mid peripheral cornea swells the RSB exhibits increased tension + compression
Tension and compression decreases compliance of the RSB
RSB markedly thins centrally
Etiology of Hyperopic Shift Biologically modulated reversible
biomechanical event Controlling elements include:
Inflammatory cytokines Change in local interstitial fluid pressures Local tissue edema Local tissue tension Local tissue compliance
Mid-peripheral edema causes localized steepening and central flattening of RSB
Flap edema caused by compliance mismatch between flap and RSB
Clinical Applications Pentacam and Optical Coherence Tomography
demonstrate no evidence of tissue necrosis Tissue necrosis is a theory not supported by any
credible data and should be categorically rejected Roberts model of biomechanics is demonstrated
to be incorrect Similar biomechanical events occur to some
degree in nearly all cases of PRK, LASIK and LASEK
A better understanding of the impact of alteration in local Pif, tissue tension and tissue compliance will have significant effects on predictability of refractive endpoints and the avoidance and management of complications