Corrosives are chemicals that can cause immediate tissue injury on contact through a chemical reaction. They are divided into acids, alkalis, and oxidants. Corrosive injury depends on factors like pH, concentration, and formulation. Common signs and symptoms include burns, pain, vomiting, and strictures. Management involves decontamination of exposed areas and prevention of late complications like strictures through steroid and antibiotic treatment. Diagnostic tests like endoscopy can assess injury grade and risk of complications.

1. INDUSTRIAL CHIMICALS:
CORROSIVES
Youan Bi Beniet Marius, Master student clin. Pharm. I
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2. OUTLINES
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INTRODUCTION
EPIDEMIOLOGY
SIGNS & SYMPTOMS
MANAGEMENT
TOXICOSIS

3.  Corrosives are a group of chemicals that have
the capacity to cause immediate tissue injury
on contact by a chemical reaction.They can
also damage or destroy metal.
 Tree types:
Acids
Alkalis
Oxidants
INTRODUCTION (1/3)
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4. INTRODUCTION(2/3)
Factors determining the corrosion potential
P H : Highly corrosive if PH is < 2 or > 11
Concentration
USE: Intended for machinery or for Hand use.
Formulation: Solid - Deep but localized injury.
Amount Ingested: > 100 -150ml – Massive poisoning
Liquid - Extensive injury
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5. INTRODUCTION(3/3)
Most commonly affect
the GIT, respiratory system, the eyes and the skin.
Corrosives=caustics something that eats away
Most common caustic agents include :
TYPE EXEMPLES
ALKALIS sodium hydroxide and
potassium hydroxide….
ACIDS hydrochloric acid, sulfuric
acid,…..
OXIDANTS Hypochlorous acids,
peroxide…..
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6. EPIDEMIOLOGY (1/3)
International poisoning statistics
estimated prevalence : 2.5-5%
morbidity : > 50%
80% occurs in children below 5 years
National poisoning statistics
Only USA are available AAPCC 2008 :
mortality : 13%
number of exposures : 191 397
poisoning attributed to caustic substances:8.6%
62.9% in children and 95.5% of all were accidental 6
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7. EPIDEMIOLOGY(2/3)
Small series available from several countries
In Kenya : Corrosives poisoning 10.8% of the
household and industrial agents (24% of all
poisoning cases) .
Some of this series gave us data on:
common corrosives used
circumstances of injury
age distribution .
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8. EPIDEMIOLOGY (3/3)
From these epidemiological data we can deduce:
children : Alkaline ingestions continue to occur
Adult : more suicidal attempts
more common in
All exposure were mostly due to alkaline.
80% are accidental
women
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9. TOXICOSIS : ROUTES OF POISONING
Major routes of exposure are:
the skin & eyes (topic)
the lung (inhalation)
the gastrointestinal tract (ingestion)
In general
Inhalation > Ingestion> Skin exposure
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10. TOXICOSIS : MECHANISM OF POISONING
Tissue injury by:
altering the ionized state and structure
disrupting covalent bonds
ion (H+) : produce toxic effects for acids
ion (OH-) : for alkaline
Pathological changes divided into 2 part :
Tissue Damage
Tissue Repair
II
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11. MECHANISM OF POISONING: PART I
TISSUE DAMAGE (1/4)
Structure of a protein Sturcture of a Phospholipid
OH & H
OH & H
_ +
_ +
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12. MECHANISM OF POISONING: PART I
TISSUE DAMAGE (2/4)
SOAP
FATS of the
cell
membrane
Proteins Proteinates
1-Proteins disruption
2-Solubilisation
3-Liquefactive necrosis
4-Further penetration
ALKALI: Acute injury, Phase I
Cell death occurs from
emulsification and disruption
of cellular membranes
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13. MECHANISM OF POISONING: PART I
TISSUE DAMAGE (3/4)
Acids: Acute injury, Phase I
No action on fats because of reverse reaction
coagulative necrosis
resulting in the
formation of an
eschar or coagulum.
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14. : tissue collagen swells
and shortens.
Responsible of edema
Inflammation
Thrombosis of the :
alkaline
ingestion :
severely injured tissues are
oropharynx, hypopharynx,
and esophagus
acid
ingestion :
commonly involved organ is
stomach
small vessels
MECHANISM OF POISONING: PART I TISSUE
DAMAGE (4/4)
& create airway
obstruction
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What complication need to be consider ?

15. MECHANISM OF POISONING: PART II
TISSUE REPAIR (1/2)
Ulceration
within 24-72 h
after acute
necrosis
Granulation
tissue replace
necrotic tissue
3-4 days of
exposure later.
Collagen
deposition
continues
for weeks
to months
Remodels
resulting in
stricture formation
Over the next 2-4
Weeks
Phase III: Fibrosis and
Stricture
Phase II: Granulation
1 2
3
4
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16. MECHANISM OF POISONING: PART II
TISSUE REPAIR (2/2)
Phase III: Fibrosis and Stricture
Fibrosis stomach Esophagus stricture
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17. SIGNS & SYMPTOMS (1/6)
 The clinical presentation depends upon:
.
the condition of exposure:
the routes of entry :
the characteristics of
the caustic agents :
Acute toxicity or chronic
toxicity ,
GIT , RT, Skin, Eyes
amount
type of the substance
Acid or alkali
physical form of
the substances
Liquid, solid,gaz
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18. SIGNS AND SYMPTOMS (2/6)
Acute toxicity : By sudden or short term exposures
GIT
acute injury
General symptoms ( pain, vomiting...)
Specifics symptoms
 Alkali
Solid form : Hoarseness & stridor
Liquid form : dysphagia & odynophagia
Acid
Epigastric pain & hematemesis.
A characteristic stain inside the mouth & lips
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19. SIGNS AND SYMPTOMS (3/6)
Late complications
GIT
Strictures and Stenosis of the esophagus
3 weeks after ingestion , in the first
three months or even after one year
Stenosis of antrum and pylorus
often 5 to 6 weeks after the ingestion.
Feeling of full stomach……GOO
Esophageal and stomach cancer
The latent period may range between 40 to
50 years.
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20. SIGNS AND SYMPTOMS (4/6)
RT
Irritation of the RT, dryness in the throat
Dyspnea
Bronchoconstriction
Pulmonary edema
Coughing
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signs & symptoms of CHEMICAL PNEUMONITIS

21. SIGNS AND SYMPTOMS (5/6)
 EYES & SKIN
Pain at the site of exposure
Burns at the site of exposure
Erythema and vesicle formation
 SYSTEMIC EXPOSURE
Ca & Mg
K
Hypotension
Dysrhythmias
Metabolic acidosis or alkalosis
2+2+
+
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22. SIGNS AND SYMPTOMS (6/6)
Chronic toxicity : by repeated exposures over a long period of time
Inhalation of certain acid
vapours cause loss of tooth
enamel, eventually leading
to extensive tooth decay
exposure to quartz-
containing dusts in the
construction industry
can cause scar tissue in
the lungs. lung suffering from silicosis
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23. MANAGEMENT
The objectif of the management of corrosives
poisoning is twofold :
Decontaminate
Prevent late complications in
case of ingestion
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The appropriate decontamination depend
upon the routes of entry

24. MANAGEMENT: DECONTAMINATION (1/4)
Occular decontamination
DO DON’T
remove the patient/victim
from the source of exposure.
Immediately flush the eyes
with large amounts of tepid
water for at least 20 minutes.
Wash eyes with saline during
transport.
Monitor the pH of the
conjunctival sac before starting
other therapeutic or diagnostic
interventions PH=7.4
Use oils, salves, or ointments
for injured eyes.
Use the gel form of calcium
gluconate in eyes
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25. MANAGEMENT: DECONTAMINATION (2/4)
Care provider should wear
gloves, water-resistant gowns,
splash resistant goggles, and masks
Remove the patient/victim from
the contaminated area.
Remove all clothing ( at least down
to their undergarments).
Thoroughly wash and rinse the
contaminated skin. using a soap and
water solution
Using hot water, strong
detergents, or harsh
abrasives
Skin decontamination
DO DON’T
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26. MANAGEMENT: DECONTAMINATION(3/4)
 GI decontamination
Ensure unobstructed airway
 Neutralization
Milk and water have been used but
their effectiveness has not been
proven. It is contraindicated.
In order to be effective, it must be
done within the first hour after
ingestion of a caustic agent.
Alkalis : mild vinegar, lemon or
orange juice.
Acids: milk, eggs or antacids;
sodium bicarbonate is not
recommended
DO DON’T
Induce vomiting (emesis)
Perform Gastric lavage
Give Activated charcoal
?
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27. MANAGEMENT: DECONTAMINATION(4/4)
 Immediately remove the
patient/victim from the source
of exposure
 Ensure that the patient/victim
has an unobstructed airway.
 Evaluate respiratory function
and pulse
 If shortness of breath occurs or
breathing is difficult
(Dyspnea), administer oxygen.
 Assist ventilation as required.
Always use a barrier or bag-
valve-mask device.
 If breathing has ceased
(apnea), provide artificial
respiration.
 Monitor the patient/victim for
signs of systemic effects and
administer symptomatic
treatment as necessary.
 Inhalational decontamination
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28. MANAGEMENT: PREVENTION OF LATE COMPLICATIONS
To prevent
Strictures
formations.
Dexamethasone 1 mg/kg/day
Prednisolone 2 mg/kg/day
Steroids
3 times a day
intravenously, given for
at least 3 weeks.
or
Antibiotics
consensus : patients treated with steroids should be
treated with antibiotics as well.
prophylactic antibiotic without steroid therapy : NO .
Pos: Ampicilline 500 mg intravenously, 6 hourly
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29. LABORATORY AND DIAGNOSTIC TESTS (1/2)
 in the acute phase of
caustic injury
 may reveal presence
of mediastinal air or
free air under the
diaphragm that may
be the evidence of
esophageal or
gastric perforation
 Perform 25–30 days
after corrosive
ingestion
 may give us useful
information on
changes in the
dimensions of
esophageal and
gastric lumen
1- Abdominal
roentgenograms
2-Esophagogastrodudodenography
with gastrographin
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30. LABORATORY AND DIAGNOSTIC TESTS (2/2)
3- Esophagogastroduedonoscopy
 For diagnostic evaluation of acute corrosive intoxications
and lesions of the upper gastrointestinal tract
 Optimal timing : the first 12–24 hours after corrosive
ingestion
 Emergency esogastroduodenoscopy depends on:
type of the corrosive
substance,
its quantity
the intention of ingestion
the corrosive substance
onset of symptoms
following the ingestion
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31. LABORATORY AND DIAGNOSTIC TESTS
– I GRADE: edema and
erythema of the mucosa,
– II A GRADE:
hemorrhage, erosions,
blisters, superficial
ulcers,
– III B GRADE:
circumferential lesions,
– III GRADE: deep grey or
brownish-black ulcers,
– IV GRADE: perforation.
– Grade 0: normal mucosa,
– Grade I: edema and erythema
of the mucosa,
– Grade II A: hemorrhage,
erosions, blisters, superficial
ulcers,
– Grade II B: circumferential
lesions,
– Grade III A: focal deep gray or
brownish-black ulcers,
– Grade III B: extensive deep
gray or brownish-black ulcers,
– Grade IV: perforation.
Kikendall
classification
Zagar classification
These classifications have enormous importance in
diagnosis and treatment of acute corrosive intoxications
.
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32. CONCLUSION
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Corrosives Contact- immediate - injury=
Children continue to be affected year after year
Corrosive is a chemical hazard in the home
Alkaline is likely to cause more damage than acid
= decontaminate and prevent lateManagement:
Prevention of corrosive poisoning is better than
complications
cure

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34. REFERENCES
 Anderson KD, Rouse TM and
al. A controlled trial of
corticosteroids in children with
corrosive injury of the
esophagus. N Engl J Med 1990;
323(10):637-40.
 Chibishev A.,Simonovska N.,
al. Post-Corrosive Injuries Of
Uppergastrointestinal Tract
Contributions, Sec. Biol. Med.
Sci., MASA, XXXI (2010); (1):
297–316
 C.P. Lakshmi, Ranjit
Vijayahari et al. A hospital-
based epidemiological study of
corrosive alimentary injuries
with particular reference to the
Indian experience .The National
Medical Journal of India 2013;
26 (1): 31.
 D.G. Nyamu, C.K. Maitai et al.
Trends of Acute Poisoning Cases
Occurring at the Kenyatta
National Hospital, Nairobi,
Kenya. East and Central
African Journal of
Pharmaceutical Sciences 2012;
15: 29-34
 D. Mignonsin, S. Yassibana Et
Al Intoxication par Les Produits
Caustiques : Etude
Epidémiologique et Approche
Thérapeutique. Médecine
d'Afrique Noire 1992 ; 39
(4) : 306-311.
 Goldman LP, Weigert JM.
Corrosive substance ingestion: a
review. Am J Gastroenterol
1984;79:85–90.
 J B Dilawari, Surjit Singh et
al. Corrosive acid ingestion in
man a clinical and endoscopic
study. Gut, 1984; 25: 183-187
 Kikendall J. Caustic ingestion
injuries. Gastroenterol Clin
North Am 1991; 220:847–57.
 Kovil Ramasamy, MD, and al.
Corrosive Ingestion in Adults J
Clin Gastroenterol 2003;
37(2):119–124.
 Lahoti D. Corrosive injury to
upper gastrointestinal tract. In:
Manual of medical emergencies,
3rd edition
 Marten Duncan, DO, Roy
K.H. Wong. Esophageal
emergencies: things that will
wake you from a sound sleep
Gastroenterol Clin N Am 2003;
32: 1035–1052
 Michael R. Macdonald et al.
Caustic esophageal burn in
children Canadian Family
Physician March 1994; 40: 559
 Moscicki ek: Gender
defferences in completed and
attempted suicides. Ann
Epidemiol 1994; 4: 152 – 158
 Paul Marchand . Caustic
Strictures of the Oesophagus.
Thorax ,1955; 10: 171.
 R Raghu Ramulu Naik , M
Vadivelan. Corrosive Poisoning
Indian Journal of Clinical
Practice August 2012; 23( 3): p31
 Scher la. Maull k.j. Emergency
management and sequelae of
acid ingestion. JACEP
1978:7:206-208.
 Zargar S.A. Kochher R, et al.
Ingestion of Corrosive Acids.
Spectrum to injury to upper
gastrointestinal tract and
natural History.
Gastroenterology 1989; 97: 702 -
707
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