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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.
Acids are substances that give hydrogen ions. The more H+ given the more strong is the acid Alkalis are substances that receive H+
Substances are commonly used for chemical assault (Vitriolage). • Assaults with caustic chemicals worldwide are more likely to occur against women
COMMONLY CORROSIVES USED • Sulphuric acid (oil of vitriol) is most commonly used . • Nitric acid & carbolic caustic soda, caustic potash has also been recorded.
Factors Affecting Severity of Injury 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.
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.
Sources Common acid containing sources common alkaline containing sources Drain cleaning products. Oven cleaning products. Swimming pool sanitizers. Automatic dishwasher detergent. Bleaches. • Toilet bowel cleaners. • Rust removing products. • Metal & cement cleaning products.
Pathophysiology Alkaline Ingestion • Deep tissue destruction • Liquefactive necrosis • denaturation and saponification of fats . • Further injury is caused by thrombosis of the blood vessels. • 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.
Acid Ingestion • Tissue injury by coagulative necrosiswith formation of coagulum or eschar. • The stomach is the most commonly involved • Esophagus being less affected because most available acids are liquids while alkalis are more commonly found as solids or pastes.
Course of the injury • Inflammatory stage: first 4-7 days, edema and erythema then thrombosis and necrosis. • granulation stage: start in about 4 days and end at 7 days by granulation tissues formation. • perforation: 7-21 days ;risk of perforation is high. • Cicatrisation (scarring): start at 3 weeks and may be persist for years, over production of scar tissue result in stricture formation.
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
Vomiting • 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. • 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.
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.
Complications of Corrosive Ingestion 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.
Chronic (Late) Complications • . Esophageal obstruction secondary to stricture formation. • Pyloric stenosis. • Malnutrition and cachexia. • Increased risk of esophageal carcinoma which occurs in 1-4% of serious caustic ingestions. • Scarring, Infection and Poor Healing may occur with Dermal Burns. • Ocular burns can result in cataract and/or complete loss of vision.
Chemical Burns Chemical burns can be caused by acids or bases (alkalis) that come into contact with tissue
Causes of death Immediate • Neurogenic shock (sever pain). • Asphyxia due to spasm and edema of glottis Late • Starvation due to stricture of the esophagus. • Pulmonary complication.
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.
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.
MANAGEMENT A. Emergency and supportive measures • Inhalation Give supplemental oxygen & observe for signs of progressive airway obstruction or noncardiogenic pulmonary edema 2. Ingestion • 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 • Do not induce emesis or attempt to neutralize the substance • 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.
. There is no specific antidote Pain Killers.
Corticosteroids • Inhibit collagen formation in wound healing. • Effective to decrease strictures if started at 24-48 hours after the burn. • 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.
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
ORGANIC ACIDS CARBOLIC ACID (PHENOL)
CARBOLIC ACID (PHENOL) • Pure carbolic acid • Colorless crystals • Specific odor • Soluble in alcohol. • The commercial forms: • Dettol /cresol /lysol /phenol
Clinical Manifestations 1. Local action: • Mild corrosive with anaesthetic effect on sensory nerve endings. b) Coagulative necrosis of the superficial layer of the tissue proteins. c) May cause skin gangrene if applied for long period. d) After ingestion there is hot burning pain extending from mouth to stomach but rapidly disappears due to local anaesthetic effect so there is no vomiting.
2. Remote action • 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
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.
Sources • Anti-rust products • Bleaches • Metal cleaners • Rhubarb lraves (نبات الراوند) amounts may cause toxicity
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 calcium oxalate resulting in: a) Arrhythmias and heart block. b) Tetany and convulsions. c) Blocking of renal tubules with calcium oxalates
Clinical Manifestations I. Local Corrosive Effect - Acid taste. - Hot burning pain (mouth, esophagus and stomach) - vomiting.
II. Remote Hypocalcemia - Tingling & numbness. - Muscle twitches in the face and extremities with carpopedal spasm. - Convulsions - Cardiac Arrhythmias • Kidney: dysuria, oxaluria, hematuria, oliguria
Chronic Exposure 1. Skin contact lead to local erosion which may lead to cyanosis and gangrene. 2. Fume inhalation may lead to renal failure.
Management Gastric lavage. Calcium should be given (Antidote) IV fluids to avoid precipitation of calcium oxalate in renal tubules.
