2.Corrosives.pptxbsjsjsjskkwkwkwjwjsbddhjdjd

Corrosive Poisons
Def.: Substances that cause destruction following
exposure to mucous membranes.
Types :
 inorganic corrosive:
acids …. H2So4, Hcl, HNo3
Alkalis ….NaoH, KoH, NH3, NH4oH
 Strong corrosives.
 Have local destructive effects:
 Through ingestion …….in the stomach.
 Through inhalation ……In respiratory system.
 through contact ………..in the skin
 Organic corrosive (Acids): carbolic & oxalic acid.
 They are mild corrosive.
 They have both local and remote action.

Corrosive Poisons
Sources & forms:
Alkalis are present in:-
 Household bleaches.
 Drain cleaners.
 Detergents e.g. automatic dishwashing.
 Cement.
Acids are present in:-
 Automobile battery.
 Metal cleaners and antirust compounds.
 Toilet bowl cleaner.

Corrosive Poisons
Industrial uses:
1. Sulphuric acid Automobile
→
battery.
2. Hydrochloric dye
→
manufacturing.
3. Nitric acid fertilizer
→
manufacturing.
4. Carbolic acid Disinfectants .
→
5. Oxalic acid metal polish & in
→
leather processing.

Inorganic corrosives (Acids)
Condition of poisoning:
Accidental: by skin contamination,
ingestion or inhalation of fumes.
Homicidal: H2SO4 acid is used for throwing
on face for disfigurement.
Suicidal: rare
Action " local action only″:
Destruction to the tissues by coagulative
necrosis severe ulcer [N.B: Mainly cause
→
perforation of stomach + skin eschars].

Clinical picture
 If ingested:
1. Severe pain from mouth to stomach; that lead to
2. Dysarthria and Dysphagia.
3. Vomiting :- black in color [shreds of stomach mucosa + acidic
heamatin]
4. Constipation.
5. Dehydration
6. Shock.
7. Decrease blood Flow to kidney [oliguria]
 If inhaled:
oedem of glottis & Asphyxia[severest from in HNO3 exposure]
 If skin exposed:
 Black eschars (H2SO4).
 Red esc hars(Hcl).
 Yellow eschars (HNO3).

Causes of death & Fatal period
1. Neurogenic shock “severe pain” …
Immediately.
2. Asphyxia …… Within few hrs.
3. Dehydration “Oligaemic shock”… within 12
hrs.
4. Perforation of the stomach …… within
days.
5. Cachexia / stricture of oesophagus ….
Within weeks
N.B: perforations is more in acids&
Cachexia is more in alkalis.

Investigations
1. Renal function tests.
2. Arterial blood gases.
3. Abdominal x-ray (perforation).
4. Fiberoptic endoscopy [for grading of
esophageal & gastric lesions] (Grades
O,I,II,III)
 Grade 0 no visible lesion
→
 Grade I Erythema + Edema(superficial)
→
 Grade II Ulceration (penetrate mucosa)
→
 Grade III → Total destruction of mucosa + Trans mural
involvement.

Treatment
If ingested:
 First Aid Measures:-
Two glasses of milk [demulcent effect] to
protect the stomach mucosa.
 Supportive measures:
Shock painkiller [e.g. Morphine].
→
Asphyxia Care of respiration [ see general]
→
Dehydration Surgical intervention [gastrectomy].
→
Cachexia Surgical intervention :
→
• colon by pass
• Oesophageal dilation[ Bougienage]

Treatment
 G.I.T Decontamination:
– No emesis, No gastric lavage, [fear of perforation
from recontact with the mucous membrane].
– No neutralisation.
– Local antidotes:
• Milk & egg white [Demulcent effect].
• H2 blockers: Ranitidine to decrease acid secretion.
 Elimination of the absorbed poison :
No need as not absorbed.
 Antidotes:
No need as not absorbed.
 Symptomatic:
Steroid to prevent fibrosis.

Treatment
If inhaled:
care of respiration [see general toxicology]
Skin exposure:
 Wash with H2o and Antibiotic
ointment.
 Skin graft may be needed.

Inorganic corrosives
(Alkalis)

(Alkalis)
Potassium hydroxide [KoH]
(caustic potash) and sodium
hydroxide [NaoH] are widely used
in houses for washing purposes
and so are common in accidental
poison in children.
Fatal dose 3-5 grams of the solid or
the corresponding amount of solution.

(Alkalis)
Accidental: Mainly
children drink Potash (K2 Co3)
which simulate milk in its color.
Action " local action only″:
Destruction to the tissues by
liquefactive necrosis severe ulcers
→
[ N.B: Mainly causes esophageal
stricture+ skin Eschars].

Clinical picture
As acids except:-
If ingested:
The mucosa of the mouth is white.
The vomitus is White & soapy [shreds of
stomach mucosa + alkaline heamatin].
Diarrhea ( white & soapy).
If inhaled:
as acids but asphyxia is more in case of
NH3 exposure.
If skin exposed: White eschars.

(Alkalis)
Causes of death & Fatal period:
as acids.
Investigations: as acids.
Treatment: as acids

Organic Acids Corrosives
Carbolic Acid (Phenol)

organic Acids corrosives
It is a coal tar derivative, in the form
of white crystals with a strong
characteristic smell.
The crude form is a solution used for
toilet disinfection.
Its other forms e.g.:
Lysol, Cresol and Dettol produce the
same effects.

 Accidental:
 Children
 Workers (absorbed through skin)
Suicidal: because of:
 Easily obtained.
 Cheap.
 Painless death.
Homicidal: Never due to characteristic
smell.

Action: local & Remote effects.
Local:
 Stomach
Mild corrosive [superficial ulcers].
Coagulative necrosis [thickening of
gastric mucosa]
Local anaesthetic action.
 Skin:
Eshars.
Local anaesthetic action.

Action: Cont.
Remote:
1. CNS: Phenols stimulate and then depress the CNS. Brief
stimulation may be related to increased acetylcholine
release, but prominent effect are CNS depression.
2. CVS: Phenols have direct myocardial depressant effect.
3. Respiration and metabolic: Phenols stimulate
respiratory centers and produce a respiratory alkalosis.
Metabolic acidosis follows because uncompensated renal
loss of base during stage of alklosis due to renal damage.
4. Methemoglobinemia: Phenol and certain phenol
derivatives (hydroquinone and coal tar) cause
methemoglobinemia.
5. Kidney: Acute glomerulonephritis.

Clinical presentations
Local:
GIT:
 Temporary burning pain from mouth to
stomach [temporary due to local anaesthetic
effect].
 Then colic and vomiting with characteristic
smell.
 Whitish buccal mucosa and brownish
carbolic eschars on lips and chin which
become brown due to oxidation.
Skin:
 whitish eschars in skin which turns brown

Clinical presentations
Remote:
1. CNS:
 constricted pupil and convulsions rapidly followed
by coma due to CNS depression& respiratory
failure.
 Central respiratory depression leads to slow
difficult respiration, cyanosis, pulmonary oedema
and death due to asphyxia after few hours.
2.CVS: Cardiovascular collapse, shock and
arrhythmias.
3. Kidney: Acute glomerulonephritis: Oliguria with
albuminuria, haematuria and casts, the urine turns to
green if left in air due to oxidation of hydroquinone

Fatal Dose:-
2-4 gm of the solid phenol or the corresponding amount
of the crude acid.
Causes of death & fetal period:
1. Within 4 hrs Respiratory failure (central asphyxia).
→
2. Within 4 days Renal failure.
→
3. Delayed death from anaemia may occur after 7-10 days.
Investigations:
1. Renal function test.
2. Urine analysis [green] look for hemoglobiuria..
3. Arterial blood gases.
4. Methemoglobin level.
5. Blood pH and electrolytes.

Treatment
Supportive measures: ABCs
 Ventilatory support/ oxygen; incubate if
necessary.
 Cardiovascular support:
A. Keep patient warm and recumbent.
B. Use IV saline and pressors to support the
blood pressure.
C. Use lidocaine for ventricular arrhythmias.
 Diazepam for seizures, if no response,
phenytoin or phenobarbitone may be given.
 Contaminated skin is washed by soap and water
then 10% alcohol followed by water.

Treatment
 GIT Decontamination:
 Emesis is not recommended due to:
 Rapid onset of coma and seizures (within half an hour for significant
ingestion).
 Corrosive action of phenol.
 Gastric lavage is indicated and essential due to:-
 Vomiting is temporary [local anaesthetic action]
 Thickening of gastric wall (coagulative necrosis) and superficial ulcers
(mild corrosive) [no fear of perforation].
 Remote action of carbolic acid, so lavage is indicated to decrease
absorbtion.
 Local antidote is:
 Milk& egg white: as phenol will coagulate their protein instead of
stomach protein.
 Magnesium sulphate15-30 gm in a glass of water to precipitate the
poison as magnesium sulphocarbonate.
 Ethanol 10% or glycerine to dissolves phenol but must be rewashed
→
to prevent absorption.

Treatment
Elimination of the absorbed poison:
Dialysis [peritoneal& hemodialysis].
No specific antidotes:
Symptomatic:
 Renal failure: Impaired renal function is treated
by 1.26% sodium bicarbonate I/V or dialysis.
 Mehemogloineima more than 30% [methylene
blue 1-2mg/kg].
 Acid-base disorders [dialysis].
 Atropine 1 mg I/V for stimulation and to
decrease pulmonary secretions.

Oxalic Acid

Oxalic acid
It is used for metal polish and
removing ink stains.
Condition of poising:
Accidental:
Mistaken by children for sugar or salt [as
it is in from of white crystals].
Occupational exposure.

Oxalic acid
Action: local& Remote effects.
Local:
 Stomach: mild corrosive [superficial ulcers]
 Skin: Eschars
Remote:
Oxalic acid combines with ionized blood calcium
forming insoluble calcium oxalate resulting in:
 Obstruction of collecting tubules by Ca oxalate crystals
which may lead to renal failure.
 Hypocalcaemia that give rise to :
• CVS: - Arrhythmias or cardiac arrest in diastole.
• Nervous system: - Tetany (peripheral).
- Convulsions (central).

Clinical presentation
 Local:
 Stomach:
 Pain & vomiting of white crystals
 Dehydration
 Skin: White eschars.
 Remote:
 Hypocalcmia:
• Twitches of the face muscles and extremities with
carpopedal spasm.
• Convulsion .
• Contraction of respiratory muscles ( Respiratory
failure).
 CVS: Arrhythmias or cardiac a systole. (fatal).
 Renal failure: - Oliguria with ca oxalate crystals in

Oxalic acid
Causes of death & fatal period:
1. Within 15 minutes due to respiratory failure
[peripheral asphyxia]
2. Within few hours from obstructive renal failure.
3. Cardiac arrest.
Investigations:
1) Renal function tests.
2) Urine analysis [white Ca oxalate crystals].
3) Ca level in blood.
4) ECG monitoring.
5) Arterial blood gases.

Treatment:
Antidote ″Ca″ is lifesaving by every route.
1) Supportive measures [ABCs]:
–Ventilatory support, oxygen and incubate
if necessary.
–Cardiovascular support:
ECG monitoring and antiarrhythmic
therapy.
2) GIT Decontamination:
Gastric Lavage + Local antidote [Milk] or
CaOH2 to precipitate oxalic acid as ca
oxalate and decrease its absorption.

Treatment:
3) Elimination of the absorbed poison:
 Dialysis.
4) Antidote:
 Ca gluconate 10 % I.V. Slowly or
orally to treat hypocalcaemia.
5) Symptomatic:
 Convulsions: Diazepam.
 I.V. fluids to prevent calcium oxalate
precipitation in the kidney.

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