Download - INDUSTRIAL CHEMICALS : CORROSIVES
INDUSTRIAL CHIMICALS:
CORROSIVES
Youan Bi Beniet Marius, Master student clin. Pharm. I
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OUTLINES
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INTRODUCTION
EPIDEMIOLOGY
SIGNS & SYMPTOMS
MANAGEMENT
TOXICOSIS
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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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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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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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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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 . 7
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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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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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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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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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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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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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: 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 ?
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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MECHANISM OF POISONING: PART II
TISSUE REPAIR (2/2)
Phase III: Fibrosis and Stricture
Fibrosis stomach Esophagus stricture
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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 17
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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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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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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
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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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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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
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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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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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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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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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 28
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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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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
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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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CONCLUSION 1
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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 late Management:
Prevention of corrosive poisoning is better than
complications
cure
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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.
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