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CORROSIVES
(CAUSTICS)
• substances which have local, rapid, &
destructive action on any tissue contacted
with.
• The generation of heat often co...
Acids are substances
that give hydrogen
ions. The more H+
given the more
strong is the acid
Alkalis are substances
that re...
• Substances are commonly used
for chemical assault (Vitriolage).
• Assaults with caustic chemicals
worldwide are more lik...
Vitriolage (chemical Assault)
Viriolage
COMMONLY CORROSIVES USED
• Sulphuric acid
(oil of vitriol) is
most commonly
used .
• Nitric acid &
carbolic caustic
soda, ...
Acids Alkalis O ther Corrosives
a) Inorganic:
sulfuric,
hydrochloric, nitric.
b) Organic:
oxalic, carbolic,
acetic
NaOH
KO...
1. Amount ingested: The more the amount the
more is the severity of the injury.
2. pH: Alkalis with pH greater than 11.5-1...
Frequency / Age
• Childhood ingestions
– Approximately 80% of caustic ingestions occur in
children less than 5Ys.
– Seriou...
Sources
Common acid containing sources
• Toilet bowel
cleaners.
• Rust removing
products.
• Metal & cement
cleaning produc...
Pathophysiology
Alkaline Ingestion
1. Deep tissue destruction
–Liquefactive necrosis
–denaturation and saponification of f...
Acid Ingestion
1. Tissue injury by coagulative necrosis
with formation of coagulum or eschar.
2. The stomach is the most c...
Course of the injury
1. Inflammatory stage: first 4-7 days, edema and
erythema then thrombosis and necrosis.
2. granulatio...
Clinical picture
• Pain
– immediate
– severe burning pain
– extending from the mouth to the stomach.
• Corrosions
– In alk...
• Vomiting
1. In alkali
• Spontaneous
• containing excessive mucus
• may be stained with dark altered blood of strongly al...
• Abdomen
– Alkali:Abdominal pain and Diarrhea ( blood stained mucoid)
– Sulphuric acid: constipation “early" due to sever...
1- Erythema, edema, erosions in the oropharynx, lips, tongue and mouth cavity.
Significant esophageal involvement may occu...
Complications of
CorrosiveIngestion
Acute Complications
1. Upper airway obstruction.
2. GIT hemorrhage.
3. Esophageal perf...
Chronic (Late) Complications
1. . Esophageal obstruction secondary to stricture
formation.
2. Pyloric stenosis.
3. Malnutr...
Chemical Burns
Chemical burns can be
caused by acids or bases
(alkalis) that come into
contact with tissue
Caustic oral burns
Caustic tongue burn
Chemical Burn
Chemical Burn
(Corneal Opacity)
Chemical Burn (Hair dye)
Causes of death
Immediate
1. Neurogenic shock (sever pain).
2. Asphyxia due to spasm and edema of glottis
Late
1. Starvati...
Imaging Studies
A) Chest & abdomen radiographs often give early clues
to mediastinits, peritonitis or severe necrosis.
B) ...
Endoscopy
• Early endoscopy in symptomatic
ingestions to define problem &
prognosis.
• Serial endoscopy is useful in follo...
A. Emergency and supportive measures
1. Inhalation
Give supplemental oxygen & observe for signs of progressive
airway obst...
. There is no specific antidote
Pain Killers.
Corticosteroids
1. Inhibit collagen formation in wound healing.
2. Effective to decrease strictures if started at 24-48 ho...
Presence of soot on face and in the
mouth especially with a facial burn
are signs of smoke inhalation.
However, these sign...
CARBOLICACID
(PHENOL)
ORGANIC ACIDS
CARBOLIC ACID (PHENOL)
• Pure carbolic acid
–Colorless crystals
–Specific odor
–Soluble in alcohol.
• The commercial forms...
1. Suicidal: Commonest form as it is
available, cheap, has local anesthetic
effect and rapidly fatal.
2. Accidental:
inges...
Phenol denatures protein
Causes coagulative necrosis
Disrupts the cell wall (protoplasmic poison)
May cause injury to the ...
The minimum toxic and lethal doses have not been well
established.
Well absorbed by inhalation, skin application, and inge...
Clinical Manifestations
2. Remote action
a. CNS stimulation followed by depression
 Headache, convulsion, drowsiness, confusion, coma.
Constricte...
Causes of Death
1. Immediate (within hours) due to central
respiratory depression.
2. Delayed (within days) renal failure....
OXALIC ACID
• Anti-rust products
• Bleaches
• Metal cleaners
• Rhubarb lraves (‫الراوند‬ ‫)نبات‬
amounts may cause toxicity
Sources
Rhubarb lraves (‫الراوند‬ ‫)نبات‬
Mode of Toxicity
1. Accidental: Commonest form
especially in children.
2. Suicidal; very rare.
Pathophysiology
1. Local mild corrosive effect.
2. Hypocalcemia: combines with blood ionized
calcium forming insoluble cal...
Clinical Manifestations
I. Local Corrosive Effect
- Acid taste.
- Hot burning pain (mouth,
esophagus and stomach)
- vomiti...
II. Remote Hypocalcemia
- Tingling & numbness.
- Muscle twitches in the face and
extremities with carpopedal spasm.
- Conv...
Chronic Exposure
1. Skin contact lead to local erosion which may
lead to cyanosis and gangrene.
2. Fume inhalation may lea...
Management
Gastric lavage.
Calcium should be given (Antidote)
IV fluids to avoid precipitation of calcium oxalate in
renal...
Button batteries
• usually cause serious injury only if they
become impacted in the esophagus, leading to
perforation into...
ALL THE BEST
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Toxicity of Corrosives

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Toxicity of Corrosives

  1. 1. CORROSIVES (CAUSTICS)
  2. 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. 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. 4. • Substances are commonly used for chemical assault (Vitriolage). • Assaults with caustic chemicals worldwide are more likely to occur against women
  5. 5. Vitriolage (chemical Assault)
  6. 6. Viriolage
  7. 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. 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. 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. 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.
  11. 11. Sources Common acid containing sources • Toilet bowel cleaners. • Rust removing products. • Metal & cement cleaning products. common alkaline containing sources • Drain cleaning products. • Oven cleaning products. • Swimming pool sanitizers. • Automatic dishwasher detergent. • Bleaches.
  12. 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. 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. 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. 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. 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. 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. 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. 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. 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.
  21. 21. Chemical Burns Chemical burns can be caused by acids or bases (alkalis) that come into contact with tissue
  22. 22. Caustic oral burns
  23. 23. Caustic tongue burn
  24. 24. Chemical Burn
  25. 25. Chemical Burn (Corneal Opacity)
  26. 26. Chemical Burn (Hair dye)
  27. 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. 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. 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. 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.
  31. 31. . There is no specific antidote Pain Killers.
  32. 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. 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
  34. 34. CARBOLICACID (PHENOL) ORGANIC ACIDS
  35. 35. CARBOLIC ACID (PHENOL) • Pure carbolic acid –Colorless crystals –Specific odor –Soluble in alcohol. • The commercial forms: –Dettol /cresol /lysol /phenol
  36. 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. 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. 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.
  39. 39. Clinical Manifestations
  40. 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. 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.
  42. 42. OXALIC ACID
  43. 43. • Anti-rust products • Bleaches • Metal cleaners • Rhubarb lraves (‫الراوند‬ ‫)نبات‬ amounts may cause toxicity Sources
  44. 44. Rhubarb lraves (‫الراوند‬ ‫)نبات‬
  45. 45. Mode of Toxicity 1. Accidental: Commonest form especially in children. 2. Suicidal; very rare.
  46. 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
  47. 47. Clinical Manifestations I. Local Corrosive Effect - Acid taste. - Hot burning pain (mouth, esophagus and stomach) - vomiting.
  48. 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. 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.
  50. 50. Management Gastric lavage. Calcium should be given (Antidote) IV fluids to avoid precipitation of calcium oxalate in renal tubules.
  51. 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
  52. 52. ALL THE BEST

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