- •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
86 |
6 Rinsing Therapy of Eye Burns |
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Fig. 6.14 Exposure of L929 cells to osmolar stable solutions with variation of pH from 11.3 to 9.5 for
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Fig. 6.15 Exposure of L929 cells to osmolar stable solutions with variation of pH from 5 to 2 for 64 min
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of the pH in the anterior chamber of the eye is much more harmful than the elevation above 9.
6.5 High End Decontamination
6.5.1 Peroxides and Radicals
Decontamination
We have found in some preliminary experiments that the decontamination of peroxides is insufficient with buffers, due to missing action on these substrates.
Therefore, we have examined drugs known for peroxide decontamination such as Dimercaprol, Vitamin C, and Tocopherol. Similar experiments were made with Diphoterine®. Our investigation aims to the restoration of the glutathione equilibrium in the exposed corneal tissue without any regeneration capacity of the tissue itself. These experiments were performed on homogenates of porcine corneas that were exposed to hydrogen peroxide and nitric acid and then treated with the different drugs. The results, given in Fig. 6.16, show a clear restoration when using Diphoterine®.
The measurements of glutathione reflect the total capacity of decontamination of oxidative stress within the cornea. The glutathione system gives the outer
6.5 High End Decontamination |
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Fig. 6.16 Glutathione |
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Fig. 6.17 The glutathione system
limits of oxidation and reduction by supplying the glutathione peroxidase with a redox potential [18] (Fig. 6.17).
All decontaminations of radicals within the body are operated by means of structural changes of ascorbate, b-carotin, or tocopherol. Those reactive partners known as the antioxidative system are all regenerated by the glutathione system. Therefore, this system gives a good overview on the oxidative state of a tissue (Fig. 6.18).
The reversal of the glutathione is not achieved by all substances and a considerable loss is produced by the agents.
The ratio of glutathione to reduced glutathione is reestablished only by Dimercaprol and Diphoterine® (Fig. 6.19).
The above-presented charts give a clear indication that none of the commercially available drugs or medical devices is able to protect the cornea from changes due to strong reducing agents or oxidants. Except this, the restoration of an equilibrium of reduced glutathione (GSH) and oxidized glutathione (GSSG) provides source of peroxidic decontamination for the tissue.
Thus with Diphoterine® and Dimercaprol, there is a considerable improvement of the physiological capacity of chemical decontamination. By this, the use of polyvalent solutions in first aid offers a considerable advantage as the best currently available treatments.
With the concept of Diphoterine®, even the restoration of glutathione contents in the burnt cornea can be achieved without any action of the regenerating tissues. This is a major value. Dimercaprol has similar effects and might be an opportune alternative, but this drug does not act on alkali and acids as well as the buffers and amphoteric substances do.
6.5.2 Hydrofluoric Acid Decontamination
In recent work, we could give proof of different decontamination strategies from conventional water rinsing over calcium gluconate to the rinsing with the specific fluoride decontaminating rinsing solution Hexa fluorine®. The specific complexation due to HF action on tissue results in the total loss of calcium within seconds as shown in cell cultures in Chap. 5 (Sect. 5.1.4, Fig. 5.9a and b). By means of photography in the ex vivo eye irritation assay and by means of Optical coherence tomography, we could give clear indication of the efficiency of the decontamination with Hexa fluorine® (Fig. 6.20).
88 |
6 Rinsing Therapy of Eye Burns |
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Fig. 6.18 Glutathione reduced content after treatment of corneal homogenate with hydrogen peroxide or HNO3
Fig. 6.19 Ratio of glutathione/reduced glutathione
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|
|
|
160 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
140 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
120 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
100 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
80 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
60 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
40 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
20 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
0 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
y |
|
O |
2 |
|
d |
|
|
|
|
|
e |
|
|
3 |
|
|
d |
|
|
|
|
e |
||
Health |
|
|
aci |
|
|
|
|
in |
HNO |
|
|
aci |
|
|
|
in |
|
|||||||
H |
2 |
|
|
|
|
|
|
|
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|
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|
|||||||
|
ascorbic |
|
+tocopherol diphoter |
|
Dimercaprol |
acorbic |
|
+tocopherol diphoter |
|
dimercaprol |
||||||||||||||
|
|
|
|
|
+ |
|
+ |
|||||||||||||||||
|
+ |
O |
2 |
|
+ |
|
|
+ |
|
|
|
HNO |
3 |
|
+ |
|
|
|
||||||
|
|
|
|
|
O 2 |
|
O |
2 |
|
|
HNO |
3 |
|
|
HNO |
3 |
HNO |
3 |
|
|||||
O |
2 |
|
H |
2 |
|
H |
2 |
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|
||||||
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|
H |
2 |
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||||||||
H 2 |
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|||||||
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|
Type of treatment |
|
|
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|
||||
6.5 High End Decontamination |
89 |
|
|
Fig. 6.20 HF burn decontamination: OCT comparison of different rinsing solutions
