- •List of Authors
- •Foreword
- •Preface
- •1.1 Burns for Doctors in Antiquity
- •1.1.1 Chemical Burns Since Antiquity
- •1.1.4 Conclusion
- •1.2 Modern History of the Chemical Burns
- •1.2.2 Start of Medical Treatment
- •1.2.4 Rinsing Therapy
- •1.2.5 Classification of Eye Burns
- •1.2.6 Specific Treatment Options
- •References
- •2.1 Introduction
- •2.2.1 Individual Publications/Case Series
- •2.2.3 US Bureau of Labor Statistics Data
- •2.3 Etiology
- •2.3.1 Work-Related Injury
- •2.3.2 Deliberate Chemical Assault
- •2.3.3 Complications of Face Peeling
- •2.3.4 Burn Center/Hospital Studies
- •2.4 Involved Chemicals
- •2.5 Conclusions
- •References
- •3.1 From Chemistry to Symptoms
- •3.1.1 What Is a Chemical Burn?
- •3.1.3 Extent of the Matter
- •3.2 The Chemical Agent
- •3.2.2.1 Acidic Function
- •3.2.2.2 Basic Function
- •3.2.2.3 Oxidizing Function
- •3.2.2.4 Reduction Function
- •3.2.2.5 Solvent Function
- •3.2.2.6 Chelating Function or Complexation
- •Energy Scale of Chelation Reactions
- •3.2.2.7 Alkylation Reaction
- •Reactivity Scale for Alkylating Agents
- •3.2.3 Modulation of the Expression of the Reactivity of a Molecule
- •3.2.3.1 Acetic Acid and Its Derivatives
- •3.2.3.2 Hydrofluoric Acid
- •3.2.3.3 Phenol
- •3.2.3.4 Methylamines Series
- •3.2.3.5 Last Illustration: Acrolein
- •3.2.4.1 Acid–Base Scale
- •3.2.4.3 Scales of Energy Level
- •3.3 Constituents of the Tissues: Which Are the Biological and Biochemical Targets?
- •3.4 The Mechanisms of the Chemical Burn During the Contact Between the Aggressor and the Eye
- •3.4.3 Key Parameters of Chemical Burns
- •Solid Form
- •Viscosity
- •Exothermic Reaction
- •Titanium Tetrachloride
- •Trichloromethylsilane
- •Boron Trifluoride
- •Sulfuric Acid
- •Concentration of the Chemical
- •Phenomenon of the Diffusion of Corrosives in Relation with Their Concentration
- •Time of Contact
- •Temperature
- •Pressure
- •3.5 Practical Conclusions in Order to Manage the Optimal Chemical Decontamination of an Eye
- •3.5.2 Consequences of a Passive Washing: A Longer Time of Action
- •3.5.3 The Concept of Active Wash
- •3.6 What is Now the Extent of Our Knowledge About Ocular Chemical Burns?
- •References
- •4: Histology and Physiology of the Cornea
- •4.1 Corneal Functions
- •4.2 Anatomy Reminder
- •4.3 Histology
- •4.3.1 The Epithelium and Its Basement Membrane
- •4.3.1.1 The Lacrymal Secretion
- •4.3.1.2 The Corneal Epithelium
- •4.3.1.3 The Superficial Cells
- •4.3.1.4 The Intermediate Cells
- •4.3.1.5 Basal Cells
- •4.3.1.6 The Basement Membrane
- •4.3.2 Bowman’s Membrane
- •4.3.3 The Stroma
- •4.3.3.1 Keratocytes
- •4.3.3.2 The Collagen Lamellae
- •4.3.3.3 Ground Substance
- •4.3.3.4 Other Cells
- •4.3.4 Descemet’s Membrane
- •4.3.5 The Endothelium
- •4.3.6 The Limbus
- •4.4 Vascularization
- •4.5 Innervation
- •4.6 Factors of the Corneal Transparency
- •4.6.1 The Collagen Structure
- •4.6.2 The Proteoglycans Function
- •4.6.3 The Absence of Vascularization
- •4.6.4 The Scarcity of Cells in the Stroma
- •4.6.5 The Regulation of the Hydration
- •4.6.6.1 The Limbus
- •4.6.6.2 The Stroma
- •4.6.7 Action of the Intraocular Pressure
- •References
- •5.1 Physiology of the Cornea
- •5.1.1 Eye Burns Physiological Barriers
- •5.1.3 Physiology of Local Decontamination
- •5.1.5 Limits between Irritation and Burn
- •5.1.6 Eye Burns
- •5.2 Pathophysiology of Eye Burns1
- •5.2.1 Types of Burns and Eye Irritation
- •5.2.2 Mechanisms of Corneal Burns
- •5.2.2.1 Contact Mechanisms
- •5.2.2.2 Thermal Contact
- •Particles
- •Hot Fluids
- •Steam
- •Liquid Metals
- •Cold Gazes
- •5.2.2.3 Eye Burns with Chemically Active Foreign Bodies
- •5.2.2.4 Eye Burns with Chemically Reactive Fluids
- •Alkali
- •Acids
- •Peroxides
- •Hydrofluoric Acid
- •Detergents/Solvents
- •5.2.3 Influence of Osmolarity
- •5.2.4 Penetration Characteristics
- •5.2.5 Cellular Survival
- •5.2.6 Release of Inflammatory Mediators
- •References
- •6: Rinsing Therapy of Eye Burns
- •6.1 Important
- •6.3 Osmolar Effects in Rinsing Therapy
- •6.3.1 Types of Irrigation Fluids
- •6.4 Effect of Irrigation Fluids
- •6.5 High End Decontamination
- •6.5.2 Hydrofluoric Acid Decontamination
- •6.6 Side Effects of Rinsing Solutions in the Treatment of Eye Burns
- •6.7 Our Expectations
- •References
- •7: The Clinical of Ocular Burns
- •7.1 Few Reminders
- •7.1.1 Anatomy Reminder
- •7.1.2 Physiology Reminder
- •7.2.1.2 Ulcer of the Cornea
- •7.2.1.3 Edema of the Cornea
- •7.2.3 The Initial Sketch
- •7.2.4.1 Signs of Alteration of the Conjunctiva
- •7.2.4.2 Signs of Intraocular Lesions
- •7.2.4.3 Extraocular Signs
- •7.3 Clinical Examination of the Evolution of Chemical Eye Burns
- •7.3.1 Benign Ocular Burns
- •7.3.2 Serious Ocular Burns
- •7.3.2.1 Complications on the Ocular Surface
- •Corneal Nonhealing
- •Other Complications on the Ocular Surface
- •7.3.2.2 Endocular Complication
- •Bibliography
- •8: Surgical Therapeutic of Ocular Burns
- •8.1 Surgical Treatment of Ocular Burns
- •8.1.3 Tenon’s Plastics
- •8.1.4 The Conjunctival Transplantation
- •8.1.6 The Transplantation of Limbus
- •8.1.6.1 Exeresis of the Conjunctival Pannus
- •8.1.6.2 The Limbus Autograft
- •8.1.6.3 The Limbus Allograft
- •8.1.8 Keratoplasties
- •8.1.8.1 Big Diameter Transfixion Keratoplasty
- •8.1.8.3 The Deep Lamellar Keratoplasty
- •8.1.8.4 The Big Diameter Lamellar Keratoplasty
- •8.1.8.5 The Keratoplasty with Architectonic Goal
- •8.1.10 Keratoprosthesis
- •8.2 Surgical Treatment of Eyelid Burns
- •8.3 Conclusion
- •References
- •9: Emergency Treatment
- •9.3.1 In Occupational Environments
- •9.3.3 Industrial Accidents
- •9.3.4 Attacks
- •9.3.5 Lack of Initial Care
- •9.4 Organizing the Emergency Chain
- •9.5.1 Emergency Chain Definition
- •9.5.2 Safety Obligations
- •9.6 Which Care Chain for Optimum Management of Chemical Eye Burns?
- •9.6.1 Immediate Care by “Nonspecialists”
- •9.6.3.1 Develop a Protocol Which Must Be Simple in Every Aspect
- •9.6.3.2 Training
- •9.6.3.3 Necessary Specialized Supervision
- •Index
74 |
5 Physiopathology of the Cornea and Physiopathology of Eye Burns |
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Fig. 5.19 VEGF after SLS corneal exposure
Dose response SLS VEGF from SM
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1200 |
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control |
1000 |
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Before burn |
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d1 |
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800 |
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d2 |
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d7 |
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to |
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compared |
600 |
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400 |
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In % |
200 |
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0 |
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3% |
6% |
15% |
30% |
Control |
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Concentration |
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structure of the cornea toward a chemical trauma. There is a considerable difference between time points of observation, types of exposure, and specific reactions of the tissue. Due to the mediator release, the response of the whole organism is triggered. Thus, prostaglandin release will cause vascular changes, itching, and pain; substance P release gives similar reactions. The interleukins result in attraction of cells from the blood vessels, and the VEGF is a strong factor of the totally undesired vascularization of the clear cornea. We can show by these experimental data that, beyond doubt, in contrast to former assumptions, the cornea itself triggers the reaction of the surrounding tissues and that the key role of treatment is to treat the release of inflammation from the cornea.
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