2. • substances which have local, rapid, &
destructive action on any tissue contacted
with.
• The generation of heat often contributes
to the damage, but they are not classic
hyperthermic burns.
• Corrosives have no remote action except
organic acids.
3. Acids are substances
that give hydrogen
ions. The more H+
given the more
strong is the acid
Alkalis are substances
that receive H+
4. • Substances are commonly used
for chemical assault (Vitriolage).
• Assaults with caustic chemicals
worldwide are more likely to
occur against women
7. COMMONLY CORROSIVES USED
• Sulphuric acid
(oil of vitriol) is
most commonly
used .
• Nitric acid &
carbolic caustic
soda, caustic
potash has also
been recorded.
8. Acids Alkalis O ther Corrosives
a) Inorganic:
sulfuric,
hydrochloric, nitric.
b) Organic:
oxalic, carbolic,
acetic
NaOH
KOH
Ammonia
Causticsauda
Lime
CaOH
a) Salts:HgChloride,
Antimonytrichloride.
b) Hydrogenperoxide.
c) Potassiumpermanganate
d) Caustichydrocarbons.
9. 1. Amount ingested: The more the amount the
more is the severity of the injury.
2. pH: Alkalis with pH greater than 11.5-12 &
acids with pH less than 2 usually cause serious
injuries.
3. Concentration: concentrated caustics are more
destructive.
4. Form of the agent: ingestion of solid pellets of
alkaline substances result in impaction in
normal anatomical sites of narrowing with
prolonged contact and may cause perforation.
5. Contact time.
10. Frequency / Age
• Childhood ingestions
– Approximately 80% of caustic ingestions occur in
children less than 5Ys.
– Serious solid ingestion is rare
– Liquid ingestions can be quite serious.
• Adult ingestion
– Most intentional ingestions occur in adults.
– Adult exposures have more morbidity than childhood
exposures because of
• significant volume
• possibility of co-ingestion of other harmful agents.
• Occupational exposures are often more severe
because industrial products are concentrated.
12. Pathophysiology
Alkaline Ingestion
1. Deep tissue destruction
–Liquefactive necrosis
–denaturation and saponification of fats .
2. Further injury is caused by thrombosis of the
blood vessels.
3. Alkalis most severely affect the squamous
epithelium of the esophagus but the stomach only
20% of cases.
Liquid alkalis multiple long strictures
Solid alkalis short dense strictures, often localized at the
level of the carina or the aortic arch, an anatomically narrow part
of the esophagus where impaction of solids occurs.
13. Acid Ingestion
1. Tissue injury by coagulative necrosis
with formation of coagulum or eschar.
2. The stomach is the most commonly
involved
3. Esophagus being less affected because
most available acids are liquids while
alkalis are more commonly found as
solids or pastes.
14. Course of the injury
1. Inflammatory stage: first 4-7 days, edema and
erythema then thrombosis and necrosis.
2. granulation stage: start in about 4 days and
end at 7 days by granulation tissues formation.
3. perforation: 7-21 days ;risk of perforation is
high.
4. Cicatrisation (scarring): start at 3 weeks and
may be persist for years, over production of
scar tissue result in stricture formation.
15. Clinical picture
• Pain
– immediate
– severe burning pain
– extending from the mouth to the stomach.
• Corrosions
– In alkali burn to lip, tongue, oral mucosa and esophagus.
Esophageal burn without oral burn may occur.
– In sulphuric acid: dark eschars at the angle of the mouth
with charring due hygroscopic action that absorb water
from tissues.
– In nitric acid: eroded tissues with yellow colour
16. • Vomiting
1. In alkali
• Spontaneous
• containing excessive mucus
• may be stained with dark altered blood of strongly alkaline
reaction (coffe ground) or brown colour due to alkaline hematin
formation.
2. In sulphuric acid:
• sever and may contain gastric contents
• dark brownish black vomitus "acid hematin".
• Mouth
Drooling with swelling of tongue, difficulty of speech and
dysphasia and corrosion.
17. • Abdomen
– Alkali:Abdominal pain and Diarrhea ( blood stained mucoid)
– Sulphuric acid: constipation “early" due to sever
vomiting and nothing pass to intestine and late due to
stricture.
• Respiratory exposure: strider, dyspnea and pulmonary
edema esp. with ammonium hydroxide and nitric acid.
• Eye exposure: distortion of mucus membrane and loss of
corneal, conjunctival and lens epithelium.
• Dermal and face exposure: burn may be noted. this
occurs esp. with sulfuric acid when thrown in the face for
disfigurement.
• Shock: due to sever dehydration with scanty urine and
collapse.
18. 1- Erythema, edema, erosions in the oropharynx, lips, tongue and mouth cavity.
Significant esophageal involvement may occur in absence of oropharyngeal lesions.
2- Early mild fever correlates with tissue necrosis.
3- Respiratory distress may be caused by aspiration mediastinitis as well as acute upper
airway obstruction.
Glottic and subglottic edema are rare and manifest as stridor and dyspnea.
4- Hypotension, tachycardia and changes in mental status signify shock.
5- Sepsis may develop shortly after presentation secondary to bacterial colonization of
dead tissue.
6- Acute peritonitis
19. Complications of
CorrosiveIngestion
Acute Complications
1. Upper airway obstruction.
2. GIT hemorrhage.
3. Esophageal perforation >Mediastinitis, Pleurisy,
Pericarditis.
4. Chemical gastritis may lead to pyloric
obstruction.
5. Gastric or intestinal > peritonitis.
20. Chronic (Late) Complications
1. . Esophageal obstruction secondary to stricture
formation.
2. Pyloric stenosis.
3. Malnutrition and cachexia.
4. Increased risk of esophageal carcinoma which
occurs in 1-4% of serious caustic ingestions.
5. Scarring, Infection and Poor Healing may occur
with Dermal Burns.
6. Ocular burns can result in cataract and/or
complete loss of vision.
27. Causes of death
Immediate
1. Neurogenic shock (sever pain).
2. Asphyxia due to spasm and edema of glottis
Late
1. Starvation due to stricture of the esophagus.
2. Pulmonary complication.
28. Imaging Studies
A) Chest & abdomen radiographs often give early clues
to mediastinits, peritonitis or severe necrosis.
B) Basic radiographic criteria with contrast studies:
1. Blurred esophageal margins secondary to mucosal
ulceration, sloughing and pseudomembrane formation.
2. Intramural retention or linear collections of the contrast
material due to deep necrotic ulcers and intramural
dissection.
3. Intralumenal retention of contrast material due to
aperistalsis.
4. Diffuse esophageal contracture due to fibrosis.
29. Endoscopy
• Early endoscopy in symptomatic
ingestions to define problem &
prognosis.
• Serial endoscopy is useful in following
patient's clinical course.
» From day 5 to 15 endoscopy should be avoided because
during this period of maximal wound softening, the risk of
perforation is increased.
30. A. Emergency and supportive measures
1. Inhalation
Give supplemental oxygen & observe for signs of progressive
airway obstruction or noncardiogenic pulmonary edema
2. Ingestion
a. Immediately give water or milk to drink.
Milk is more preferable than water because milk forms a blanket of
protein precipitate and limits the damage to mucosal surface
b. Do not induce emesis or attempt to neutralize the substance
c. If esophageal or gastric perforation is suspected, obtain
immediate surgical or endoscopic consultation.
3. Dermal exposure: irrigation with tap water after removal of
contaminated clothes.
4. Eye exposure: Copious irrigation with water.
32. Corticosteroids
1. Inhibit collagen formation in wound healing.
2. Effective to decrease strictures if started at 24-48 hours
after the burn.
3. Recommended in 2nd. degree burns because:
1st. degree burns rarely if ever cause strictures.
3rd. degree burns almost cause strictures and the use of corticosteroids
may decrease frequency and severity of strictures but they also may
mask infection, promote tissue softening thus possibly increase
frequency of perforation by softening wounds.
Contraindications:
1. Evidence of perforation. 2. GI bleeding. 3. Delayed presentation.
33. Presence of soot on face and in the
mouth especially with a facial burn
are signs of smoke inhalation.
However, these signs can be absent
in the presence of significant smoke
injury.
Massive facial edema can
be anticipated with a
facial burn especially
involving lips and mouth.
Early endotracheal
35. CARBOLIC ACID (PHENOL)
• Pure carbolic acid
–Colorless crystals
–Specific odor
–Soluble in alcohol.
• The commercial forms:
–Dettol /cresol /lysol /phenol
36. 1. Suicidal: Commonest form as it is
available, cheap, has local anesthetic
effect and rapidly fatal.
2. Accidental:
ingestion in children
or absorption
through the skin.
37. Phenol denatures protein
Causes coagulative necrosis
Disrupts the cell wall (protoplasmic poison)
May cause injury to the eyes, skin & respiratory tract.
Systemic absorption causes CNS stimulation (unknown
mechanism) followed by depression.
Some phenolic compounds (eg, dinitrophenol) may induce methemoglobinemia.
38. The minimum toxic and lethal doses have not been well
established.
Well absorbed by inhalation, skin application, and ingestion
Inhalation
250 ppm is considered immediately dangerous to life or health (IDLH)
Skin application
• Death has occurred in infants from repeated dermal applications of small doses
(one infant died after a 2% solution of phenol was applied for 11 hours on
the umbilicus under a closed bandage).
• Solutions >5% are corrosive.
Ingestion
• Deaths have occurred after adult ingestions of 1–32 g of phenol
• As little as 50–500 mg has been reported as fatal in infants.
40. 2. Remote action
a. CNS stimulation followed by depression
Headache, convulsion, drowsiness, confusion, coma.
Constricted pupil.
b. Respiratory depression
c. Heart: myocardial
d. Kidney: acute glomerulonephritis with oliguria,
albuminuria, casts, anuria and renal failure.
Urine turns dark green on exposure to air
due to oxidation of the excreted products
of phenol
41. Causes of Death
1. Immediate (within hours) due to central
respiratory depression.
2. Delayed (within days) renal failure.
Management
1. Care of respiration and coma if present.
2. Gastric lavage may be done in early presentation.
3. Symptomatic treatment and dialysis if renal failure
occurs.
4. Skin lesions irrigated with water.
45. Mode of Toxicity
1. Accidental: Commonest form
especially in children.
2. Suicidal; very rare.
46. Pathophysiology
1. Local mild corrosive effect.
2. Hypocalcemia: combines with blood ionized
calcium forming insoluble calcium oxalate
resulting in:
a) Arrhythmias and heart block.
b) Tetany and convulsions.
c) Blocking of renal tubules with calcium
oxalates
48. II. Remote Hypocalcemia
- Tingling & numbness.
- Muscle twitches in the face and
extremities with carpopedal spasm.
- Convulsions
- Cardiac Arrhythmias
- Kidney: dysuria, oxaluria, hematuria,
oliguria
49. Chronic Exposure
1. Skin contact lead to local erosion which may
lead to cyanosis and gangrene.
2. Fume inhalation may lead to renal failure.
51. Button batteries
• usually cause serious injury only if they
become impacted in the esophagus, leading to
perforation into the aorta or mediastinum.
• Most cases involve large (25-mm diameter)
batteries.
• If button batteries reach the stomach without
impaction in the esophagus, they nearly always
pass uneventfully via the stools within several
days
