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

following the ingestion 30

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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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