- •Foreword
- •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
9.6 Which Care Chain for Optimum Management of Chemical Eye Burns? |
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For the irritating or corrosive chemicals we are concerned with here, the top priority is to break the “product– human tissue” contact. This can be done in two ways:
•Through spontaneous mechanical entrainment by the victim or by the witnesses: wiping, washing with copious amounts of water
•By fully neutralizing the product by chemical means (“antidote effect”)
9.5.3 The Specific Management
of Chemical Injuries
Any attempt to administer care after an accident or chemical aggression is doomed to failure if it is impossible to “remove” the aggressive product (or move away from it).
On the other hand, any procedure and any “neutralizer” that prevents or effectively reduces the time of contact with the eye as soon as the chemical nature of the aggression is recognized will be beneficial.
Therefore, it is obvious that, to apply these principles and use this “neutralizer” as soon as possible, the emergency procedure should be well known to everyone and sufficiently simple. In addition, to avoid any loss of time, the “neutralizer” should always be available near the risk.
Once the aggressive product is “neutralized,” in the broad sense of the term, than medical care can begin. In all cases of chemical eye injury, medical advice should be sought as soon as possible.
eye burns is “either it is not serious and it will heal, or it is very serious, and there is nothing we can do.” Now, it is the ophthalmologist’s expertise which will dictate the course of action to be taken. This biased assessment of the problem led to the implementation of treatment strategies, which are interesting but have limitations.
9.6.1 Immediate Care by “Nonspecialists”
First limitation: immediate care is administered to the victim by nonspecialists, or even non-healthcare people. Now, there has been one dogma in France for several decades: a chemical eye burn means washing with water and, above all, not using anything else, especially no “neutralizing” solutions.
This course of action has unquestionable clinical and experimental arguments but only when action is taken during the very first seconds after the corrosive chemical splash. Water rinsing has only a mechanical action, entraining the chemical out of the eye. Therefore, it will simply reduce the number of potential chemical aggressors on ocular tissue.
After one minute, however, all the experimental studies have demonstrated the ineffectiveness and even harmfulness of eye rinsing with water or with the other isotonic solutes (isotonic to blood). In fact, these aqueous solutions dilute the chemical substance and facilitate the release of the active ions of the corrosive or irritating product. In addition, being hypoosmolar to the cornea, aqueous solutions create flows from tissue surface to the inside, favoring the penetration of the chemical into ocular tissue (see Chaps. 5 “Physiopathology” and 6 “Eye Rinsing Solutions”).
9.6 Which Care Chain for Optimum Management of Chemical
Eye Burns?
The management of chemical eye burns is not the sole concern of the ophthalmologist. It takes often several hours between the burn and the visit to the ophthalmologist. During this time, many treatments have been administered, or most often, not administered because they have not been approved by the specialist. Therefore, at the time of the visit to the ophthalmologist, the prognosis is already settled. Here, we have a vicious circle: the most common vision ophthalmologists have of chemical
9.6.2 Ophthalmological Management
is Often Deferred
This is the second limitation of common treatment strategies. For specialist care to victims of chemical eye injuries, ophthalmologists, especially French ophthalmologists, have developed since quite a long time more or less complex surgical strategies to attend to restore sight to severely burnt people: corneal grafting, limbal autograft or allograft, amniotic membrane grafting, and keratoprosthesis.
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9 Emergency Treatment |
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9.6.3 Practical Consequences
for More Effective Management
In addition to these specialist treatments that are relatively late with the reference to the initial chemical splash, there remains ample room for another treatment objective aimed at avoiding or limiting the immediate seriousness of a chemical eye.
To achieve this aim, you need a real eye burn management chain. In reality, many persons will give aid to the burnt person before he/she meets the ophthalmologist. Therefore, the setting up of an eye burn care chain is possible. The difficulty will be to have persons who are most often unqualified administer initial care. This is possible, on the basis of our experience, under three conditions: a good protocol, suitable training, and technical supervision by healthcare professionals.
9.6.3.1 Develop a Protocol Which Must Be Simple in Every Aspect
•Understandable in view of the desired therapeutic action, in order to gain acceptance by the person who is to use it
•Easy to implement, by simple decision-making because of the absence of any contraindication and side effect
•Easy and very quick to implement
9.6.3.2 Training
Training will be essential for the persons who are to implement the protocol. This training shall be given initially and regularly updated. It will combine theoretical aspects and especially practical situations consistent with the type of risk.
9.6.3.3 Necessary Specialized Supervision
This is the third and last condition to achieve a credible, effective system. The action should be supervised by recognized healthcare professionals, so that it is professionally credible and follow-up can be ensured to take account of the results and improve the relevance and quality of the implemented system.
Index
A |
phenol, 23–24 |
Acidic buffering, 62 |
molecular structure, irritant/corrosive, 18–19 |
Acidic function, 19 |
reactive functional groups, irritant/corrosive agents |
Acrolein, 24–25 |
acidic function, 19 |
Active wash, 44–46 |
alkylation reaction, 21–22 |
Alkylation reaction, 21–22 |
basic function, 19 |
Allograft, 106–109, 117 |
chelating function/complexation, 21 |
American Association of Poison Centers, 10 |
molecular reactivity and chemical bonds, 22 |
Amniotic membrane, 106 |
oxidizing function, 19–20 |
Aqueous humor, 61 |
reduction function, 20 |
Autograft, 98, 100, 105–108, 117 |
solvent function, 20–21 |
|
types of chemical reactivity, 18 |
B |
Chemical assault, 11–13, 17, 32 |
Basal cells, 51–52 |
Chemical concentration, 39–40 |
Basement membrane, 52 |
Chemical emergency, 113–114 |
Basic function, 19 |
emergency care |
Benign ocular burns, 99 |
active wash, 44–46 |
Boron trifluoride, 37–38 |
consequences of passive washing, 44 |
Bowman’s membrane, 52 |
dilution and mechanical draining, 43–44 |
Buccal mucosa transplantation, 104–105 |
Chemical trauma, 113 |
|
Clinical signs |
C |
complications, on ocular surface |
Cataract, 101 |
corneal nonhealing, 99–100 |
Cederoth, 83, 90 |
ectropium-trichiasis of, 101 |
Cellular survival, 71 |
symblepharons, 100–101 |
Chelating function, 21 |
conjunctival alteration, 98 |
Chemical agents and reactions |
corneal edema, 96–97 |
biological and biochemical targets, 29–31 |
corneal ulceration |
chemical burn knowledge, 46–48 |
superficial punctuate keratitis, 96 |
chemical burns, 17 |
endocular complications, 101 |
parameters affecting chemical burns, 17 |
extraocular signs, 99 |
elementary reactivity, 18 |
intraocular lesions, 98–99 |
energetic levels of chemical reactivity |
perilimbal (conjunctival) ischemia |
acid–base scale, 25–28 |
alkali, 95, 96 |
irritant, 27 |
hyperhemia of, 95 |
scales of, 27, 29 |
limbus, 94, 95 |
mechanisms of chemical burn |
upper conjunctival ischemia, 96 |
energy dimension, 33–34 |
Roper Hall’s Prognostic classification, 97 |
parameters, 34–39 |
Cold gaze burns, 67 |
risk factors, 39–43 |
Collagen lamellae, 52, 53 |
types of chemical reactivity, 31–33 |
Conjunctiva |
modulation, reactivity of molecule |
ischemia, 94–96 |
acetic acid and derivatives, 22–23 |
pannus, exeresis, 105 |
acrolein, 24–25 |
transplantation, 104 |
hydrofluoric acid, 23 |
Cornea |
methylamines series, 24 |
anatomy, 49, 93 |
119
120 |
Index |
|
|
burns, mechanism of
with chemically active foreign bodies, 67–68 with chemically reactive fluids
acids, 68 alkali, 68
detergents/solvents, 70 hydrofluoric acid, 70 peroxides, 68–70 thermal contact, 67
calcifications, 90 edema, 96–97 histology
Bowman’s membrane, 52 descemet’s membrane, 53 endothelium, 53–54
epithelium and basement membrane, 49–52 limbus, 54–55
stroma, 52–53 innervation, 55 leucoma, 101 nonhealing, 99–100 osmolarity, 56, 79, 82 pathophysiology of
decontamination on eye, 59–61 eye burns physiological barriers, 59 impregnation, 65, 66
irritation and burn, 64–65
limits of physiological decontamination, 63–64 local decontamination, 60–63
scratched, 90 transparency, 93–94 transparency, factors of
collagen structure, 55 intraocular pressure, 57 proteoglycans function, 55 recovery mechanism of, 56–57 regulation of hydration, 55–56 scarcity of cells in stroma, 55
ulceration, 98 fluorescein with, 96
superficial punctuate keratitis, 96 vascularization, 55
Corrosives
diffusion of, 40–41
time of contact, with eye, 41–42
D
Decontamination active d, 55
chemical d, 18, 43–46, 87 emergency d, 18
initial d, 9
Deep lamellar keratoplasty (DLK), 108 Descemet’s membrane, 53
Dilution and mechanical draining, 43–44 Diphoterine®, 36, 45, 71, 77–84, 87, 115
E
Ectropium–trichiasis, 101
Edema, of cornea, 96–97
Emergency care
active wash, 44–46
consequences of passive washing, 44 dilution and mechanical draining, 43–44
Emergency chain, 116 Emergency treatment
chemical emergency, 113–114 chemical ocular traumas, characteristics
and consequences, 113 first aid management, 114–115
management of chemical eye burns care by nonspecialists, 117
ophthalmological management, 117–118 ocular injury treatment
emergency chain definition, 116 safety obligations, 116–117
Endocular inflammation, 101 Endothelial cells, 53–54
Endothelium, 7, 53–56, 59, 70, 71, 78, 79, 82, 93, 108 Energetic levels
acid–base scale, 25–28
irritant power of acids/bases, 27 scales of chemical reactions, 27, 29
Epidemiology, 9–14 Epidemiology, of injuries
data limitations and scope
American Association of Poison Centers NDPS, 10 burn center/hospital studies, 13–14
individual publications, 9–10 occupational burn data, 9
US Bureau of Labor Statistics data, 10 work-related injury, 11
etiology
chemical substances, 14 complications of face peeling, 13 deliberate chemical assault, 11–13
Epithelium, of cornea basal cells, 51–52 intermediate cells, 51
lacrymal secretion, 49–50 necrosis, 97
superficial cells, 50–51 Exothermic reaction, 36 Extraocular signs, 99
Eyelid burns, surgical treatment, 109–110
F
Face peeling, 13
First aid management, 114–115
G
Glucose, 30, 31
Glutathione system, 86–88
Guy de Chauliac, 2
H
Hexafluorine®, 38, 70, 87, 90, 114 Hippocrates Heraclidae, 3
History, of chemical burns and relative treatments, 3–4 eye burns, classification of, 6
Guy de Chauliac, 2 Hippocrates Heraclidae, 3
Index |
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intensive care revolution, thermal burns and, 4–5 Marcel Legrain, 4
medical treatment, 6 origins, 5–6 reconstitutive concepts, 7 rinsing therapy, 6
skin burns, 5
toxicology and ophthalmology, research in, 6 treatment options, 7
Hydrofluoric acid (HF), 21, 28 burn mechanism, 33 decontamination, 87, 89–90 eye burns with, 70
pH, 26, 27 reactivity of, 23 rinsing therapy
decontamination, 87, 89–90 diffusion, 78
Hypertonic, 46, 56, 114
I
Inflammatory mediators
dose response SLS IL-8 from SM, 72, 73 eye burn model, 72
interleukin-8, 72 VEGF
NaOH corneal exposure, 72–73 SLS corneal exposure, 73–74
Innervation, 55 Intraocular lesions, 98–99 Intraocular pressure, 57
Irrigation fluids, rinsing therapy effect of
anterior chamber pH, 83 buffer capacity, 84
electrolytic contents, comparison of, 83 intracameral pH after corneal rinsing, 85 L929 cell, 85–86
types of, 82 Irritant/corrosive chemicals
molecular structure of, 18–19 reactive functional groups
acidic function, 19 alkylation reaction, 21–22 basic function, 19
chelating function/complexation, 21 molecular reactivity and chemical bonds, 22 oxidizing function, 19–20
reduction function, 20 solvent function, 20–21
K
Keratocytes, 52–53 Keratoplasty
with architectonic goal, 109 lamellar keratoplasty, 108–109
transfixion keratoplasty (TK), 106–108 Keratoprosthesis, 109
L
Lacrymal secretion, 49–50 Lacrymal, 113, 114
L929 cells, irrigation fluids effect, 85, 86 Limbal stem cells (LSC), 105
Limbus
corneal regenaration, 56
epithelial cells, transplantation, 109 histology, 54–55
transplantation allograft, 106 autograft, 105
conjunctival pannus, exeresis of, 105 Lipids, 30, 31
Liquid metal burns, 67
M
Marcel Legrain, 4
Methylamines series, 24
N
Nasal mucosa transplantation, 104–105 National Poison Data System (NDPS), 10 Necrotic tissues, debridement/excision, 103
O
Ocular anatomy and physiology, 93–94 Ocular hypertonia, 101
Osmolar effect, 78–82 Osmolarity
effects, rinsing therapy, 78–82 eye burns pathophysiology, 70–71
Oxidizing function, 19–20
P
Passive washing, 43–44 Pathophysiology, of eye burns
cellular survival, 71
corneal burns, mechanisms of, 66–70 inflammatory mediators, 72–74 osmolarity, 70–71
penetration characteristics, 71 physiological barriers, 59
Perilimbal ischemia, 94–96 Peroxides, 68–70
Phenol, 23–24
Plum, 83, 84, 90 Pressure, 43 Proteins, 30, 31
buffer, 60 Proteoglycans, 55
R
Reactive functional groups, irritant/corrosive agents acidic function, 19
alkylation reaction, 21–22 basic function, 19
chelating function/complexation, 21 molecular reactivity and chemical bonds, 22 oxidizing function, 19–20
122 |
Index |
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reduction function, 20 solvent function, 20–21
Reduction function, corrosive agents, 20 Ringler, 81, 83, 84
Rinsing therapy development, issues in, 91
diffusion, mechanisms of, 78 glutathione system, 86–88 history, 6
hydrofluoric acid decontamination, 87, 89–90 irrigation fluids, effect of
anterior chamber buffer capacity, 84
electrolytic contents, comparison of, 83 intracameral pH after corneal rinsing, 85 L929 cell, exposure of, 85, 86
osmolar effects in blown-up cells, 81 corneal stroma, 79 corneal swelling, 82
cytolysis and necrosis, 120 s of exposure with, 81 Diphoterine®, 82
irrigation fluids, types of, 82
tissue culture, with 800 mOsmol (NaCl), 81 water contents of, 80
side effects of
corneal calcifications, 90 scratched cornea, 90
S
Safety obligations, 116–117 Sodium lauryl sulfate (SLS), 72–74 Solvent function, 20–21
Stem cell, 71, 91, 95, 96, 98, 100, 104, 105, 109 Stroma, 59, 78-80, 97, 107-109
collagen lamellae, 53 corneal regeneration, 57 ground substance, 53 keratocytes, 52–53 scarcity of cells in, 55 Schwann cells, 53
Sulfuric acid, 39, 40 Superficial cells, 50–51
Supernatant rinsing medium (SM), 72–74 Surgical treatment
of eyelid burns
in critical phase, 110
in sequelar phase, 110 keratoprosthesis, 109 lamellar keratoplasty (LK)
big diameter, 108–109 deep, 108
necrotic tissues, debridement/excision of, 103 symblepharons formation, prevention of, 103 Tenon’s plastics, 103–104
transfixion keratoplasty (TK) big diameter, 106–107 usual diameter, 107–108
transplantation
amniotic membrane, 106
buccal and nasal mucosa, 104–105 conjunctival, 104
cultivated limbal epithelial cells, 109 limbus, 105–106
Symblepharons, 12, 98, 100, 101, 103, 104, 106
T
Tear fluid, 61 Temperature, 42–43 Tenon’s, 55, 103–105 Tenon’s plastics, 103–104 Thermal eye burns, 67
Tissue culture, in rinsing therapy with Diphoterine®, 82
with 800 mOsmol (NaCl), 81 Titanium tetrachloride, 36–37 Transplantation
amniotic membrane, 106
buccal and nasal mucosa, 104–105 conjunctival, 104
cultivated limbal epithelial cells, 109 limbus, 105–106
Trichloromethylsilane, 37
U
US Bureau of Labor Statistics, 10
V
Vascularization, 55
Vinegar, 22–23
Viscosity, 35–36
W
Work-related injury, 11
