- •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
7.3 Clinical Examination of the Evolution of Chemical Eye Burns |
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applanation tonometer dangerous (risk of infection). It can now be done with lower risks of infection thanks to the use of an air-puff tonometer. In general, the ocular pressure is normal in the initial step.
7.2.4.3 Extraocular Signs
Most of the times, chemical eye burns are due to projections of chemicals to the face. It is important that the initial clinical analysis mentions the associated clinical signs, as far as the circumstances of the chemical burn often give them a medicolegal interest. These signs may be:
•Palpebral burns
•Face burns, the depth of which is to be estimated as first, second, or third degree. As these hurts are caused by liquid substances, in general, the burns are a little deep but really extended.
•Burns of the lacrymal system. They are uneasy to evaluate, however looking for a stenosis of the lacrymal point or canaliculi is essential. Concerning serious chemical eye burns, a systematic wash of the lacrymal system also enables to check its permeability.
•Burns of the nose mucous membrane, because of the chemical passing through the lacrymal system. It is necessary to do a nasal examination no later than the next day after the accident.
•Burns of the lips and mouth mucous membrane
7.3 Clinical Examination of the
Evolution of Chemical Eye Burns
There are two types of evolution.
7.3.1 Benign Ocular Burns
Benign ocular burns are grade 1 and grade 2 ocular burns. They evolve toward healing within 10 days or so. In this case, the epithelium of the cornea centripetally and gradually grows back. Treatments aim to prevent infectious complications and to support cicatrization.
7.3.2 Serious Ocular Burns
Serious ocular burns are grade 3 and grade 4 ocular burns. After primary alteration of the ocular biological tissues by the chemical, some biological reactions of cicatrization develop. As in any cicatrization, there are two phases: the detersion phase to eliminate the altered tissues and the repairing phase. Serious eye burns modify these two phases: they increase the ability of detersion and reduce the ability of reparation. Such a cicatrization then takes several weeks or months until consolidation of the lesions.
7.3.2.1 Complications on the Ocular Surface
Corneal Nonhealing
The absence of corneal cicatrization is illustrated by a recurrent ulcer of the cornea that will first reduce then form again and never heal (Fig. 7.12).
At such a step and every 48 h, there must be a thorough clinical examination of the corneal edema, because it is certainly a cause of the noncicatrization of the cornea. A good illustration of this phenomenon is the image of a roof collapsing because it is supported by a too weak structure. The epithelial
Fig. 7.12 Recurrent ulcer of the cornea after ocular burn by alkali (12.8% ammonia, pH = 11.5)
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7 The Clinical of OcularBurns |
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cells and particularly their basement membrane cannot be supported by a corneal stroma with edema. This clinical notion has a therapeutic interest: the use of anti-inflammatory and corticoid drugs to reduce and eliminate the edema. But these drugs have an inhibitive effect on the back growth of the epithelium, so they must be stopped as soon as the edema reduces, whereas the prescription of medicines facilitating the epithelialization must be increased. On the other hand, the stromal edema is not the only cause of the development of a marginal ulcer. The lack of limbal stem cells is also a primordial element of the evolution of this pathology. The evaluation of the remaining capital of the burnt eye is indirect and rough, and based on the observations of the initial examination. At this stage, while considering the rest of the ocular state, an autograft of limbus or a graft of amniotic membrane can be proposed.
The spontaneous evolution of this type of ulcer is dramatic and within a few weeks results in the conjunctival covering. This phenomena begins in the zone where limbal stem cells are the most insufficient, that is, as a general rule, in the inferior part. It gradually develops over the entire corneal surface and finally results in a complete conjunctiva that is completely covered and a loss of visual function of the damaged eye (Figs. 7.13 and 7.14).
The noncicatrization of the ulcer may also result in a spontaneous puncture of the cornea (Fig. 7.15).
Fig. 7.14 Old conjunctival covering due to eye burn. The patient perceives the light
Fig. 7.13 Beginning of a conjunctival covering after eye burn by alkali (12.8% ammonia, pH = 11.5)
Fig. 7.15 Spontaneous puncture of the cornea after eye burn by alkali (12.8% ammonia, pH = 11.5) with numerous symblepharons completely preventing the opening of the eyelids
Other Complications on the Ocular Surface
There might be other complications on the ocular surface like:
•Abscess of the cornea, which must be systematically prevented by checking the antitetanic vaccination and the prescription of local therapies by antibiotics.
•Symblepharons, which must also be systematically prevented by the installation of a symblepharon
