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9.6  Which Care Chain for Optimum Management of Chemical Eye Burns?

117

 

 

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.

118

9  Emergency Treatment

 

 

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

121

 

 

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

 

 

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