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• 1.Epidemiology
• The incidence of corrosive esophagitis which caused by ingested
strong acids, strong bases, a bleach solution is estimated to be about
3-5% of cases of accidents and suicides or about 5,000-10,000 cases
per year in the United States. Children under 5 years reported
frequent ingestion of substances that are corrosive due to accident
and neglect. While in adolescents and adults reported cases quite
often in adolescents as suicide attempts. There are no sex and race
differences that influence corrosive esophagitis.
• 2.Etiology
• Corrosive esophagitis is most often caused by ingestion of household
cleaning agents, usually by children. The most damaging substances
are sodium hydroxide, or which causes tissue lysis and often
penetrate the esophageal wall. The channel cleaner fluid may damage
the esophagus or cause lesions.
• Symptoms are exacerbated by alcohol use, smoking, poor lifestyle and

• 3.Pathogenesis
• Caustic substances such as strong acids and strong bases damage body tissues by altering
the structure of ions and molecular structures and disrupting covalent bonds in cells.
• 1. Strong base
• The strong base binding causes the tissue necrosis to melt (liquefactumnecrosis), a
process involving fat saponification and protein solubilization. Cell death is caused by
emulsification and destruction of cell membrane structures. The hydroxy ion (OH-)
derived from the basic agent reacts with the collagen tissue resulting in swelling and
tissue shortening (contracture), thrombosis of the capillary vessels, and tissue heat
• The tissues most frequently exposed to the first contact by a strong base are the
oropharyngeal squamous epithelial layer, the hypopharynx, and the esophagus. The
esophagus is the organ most frequently affected and the most severe level of damage
when ingested strong base compared to the stomach, In 48 hours of tissue udem that
can cause airway obstruction, then within 2-4 weeks can form stricture.
• 2. Strong acids
• The tissue damage due to ingestion of strong acids is coagulation
necrosis, there is a process of denaturation of superficial proteins that
will cause clot, crust or scab can protect the underlying tissue from
damage. The stomach is the organ that is most often exposed in the
case of ingested strong acids, in 20% of small bowel cases can also be
affected. Scab and clot proteins formed peel within 3-4 days replaced
by granulation tissue, tissue perforation can occur in this process. The
acute complications that occur are, vomiting resulting from pyloric
spasm, perforation and gastrointestinal bleeding.
• 4.Clinical manifestation
• Corrosive eosfagitis according to degree of burns can be divided into:
• 1. corrosive esophagitis without ulceration
• Patients experience mild swallowing disorders. On esophagoscopy appears hyperemic mucosa without ulceration.
• 2. Corrosive esophagitis with mild ulceration
• Patients complain of mild dysphagia, in an ulcer-indistinct esophagoscopy, confined to the mucosal lining only.
• 3. Serious ulcerative corrosive odfagitis
• Ulcers are already about the muscle layer, usually found one ulcer or multiple.
• 4. Severe ulcerative corrosive ulceration without complications
• There is exfoliation of the mucosa and necrosis that lies in, and has been about all the lining of the esophagus. This condition if left
unchecked will cause oesophageal stricture.
• 5. Severe ulcerative corneal complications with complications
• There is perforation of the esophagus that can cause mediastinitis and peritonitis. Occasionally encountered signs of upper
respiratory tract obstruction and acid base balance disturbance.

• 5.Diagnosis
• 1. Anamnesis
• Based on anamnesis enforced with the history of ingested corrosive substances
or organic substances, and shown by the main complaints of patients feeling
burning in the esophagus, painful pain, and difficult to swallow.
• 2. Physical Examination
• The entry of corrosive substances through the mouth can be known by bad
breath or vomit. The presence of whitish burns on the mucosa of the mouth or
gray on the lips and chin shows due to caustic or corrosive material either strong
or strong acid. Differences in the impact of burns are coagulative necrosis due to
strong acid exposure while strong bases result in nuisance of the liquid.
• 3. Pemeriksaan penunjang????
• Might be done with laboratory, radiologic, esophagoscopy.
• 6.Therapy
• 1) Emergency maintenance treatment.
• a. Monitoring of vital signs, airway, heart, and IVFD installation, CaCl 2 administration in patients swallowed with hydrogen fluoride
substances may prevent cardiac arrest due to hypocalcemia.
• b. Control of the airway, as it may occur udem on the airway, the monitoring should be as soon as possible, equipment for
intubation or tracheostomy should be ready.
• c. Gastric emptying and decontaminacid.
• d.Surgery is performed immediately if there is perforation, mediastinitis oruperitonitis.

• 2) Pharmacology
• a. Cephalosporin class antibiotics such as ceftriaxone have a broad antibacterial spectrum against gram positive and gram
• b. Proton pump inhibitor preparations such as omeprazole and pantoprazole can reduce the exposure of gastric acid to the
esophagus that can reduce the risk of stricture.
• c. The use of corticosteroids should be considered because studies show that stricture formation occurs based on the degree of
tissue damage.
• 7.Complications
• 1. Edema and airway obstruction.
• 2. Gastroesophageal perforation.
• 3. Mediastinitis, pericarditis, pleuritis, tracheoesofageal fistel, esophageal-aorta
fistula, and peritonitis.
• 4. Stricture formation within 2-4 weeks.
• 5. Gastric gastric obstruction to the duodenum
• 6. Gastrointestinal tract.
• 7. Symptoms of systemic poisoning due to absorption of substances into the
• 8. Cardiac arrest due to hypocalchemical effects of hydrogen fluoride.
• 9. Squamous cell carcinoma, can occur within 40 years after exposure
• Prognosis
• The prognosis depends on the degree of burns experienced by the patient,
as well as the type of ingested ingredient, the duration of exposure, Ph,
volume, concentration, ability to penetrate the tissue, as well as the
amount of tissue damage necessary to neutralize the incoming substances.
• The mortality rate ranges from 1-4% due to effective surgical techniques,
anesthesia, antibiotics, and nutrients, death is generally caused by
mediastinitis, peritonitis, sepsis, malnutrition, aspiration, and failure of the
organs’ functions.