| Grade |
Appearance |
Clinical Significance |
| 0 |
Normal |
PO fluids immediately |
| I |
Erythema, edema, loss
of normal vascular pattern |
Temp dysphagia, can
swallow within 0-2 days, no long term sequelae |
| IIa |
Transmucosal injury
with friability, hemorrhage, blistering, exudate,
superficial ulceration |
Scarring, no stenosis,
no long term sequelae |
| IIb |
Circumferencial or deep
ulceration (ulceration > 1/3 length of esophagus) |
small risk of
perforation, scar may result in later stenosis |
| IIIa |
Circumferential,
scattered deep ulceration (necrosis <1/3 length of esophagus) |
Risk of perforation,
Hi-risk of later stenosis |
| IIIb |
Extensive necrosis (necrosis >1/3 length of esophagus) |
Hi-risk for perforation
and death, Hi-risk of stenosis |
Esophageal injury in children can result from mechanical trauma, caustic ingestion, or medication-induced damage. Caustic ingestion is most common between ages 1 to 3 years, often due to accidental exposure to household cleaning products. Esophageal burns occur in 18%–46% of such cases, with alkali agents—such as oven cleaners, drain cleaners, and dishwasher detergents—being the most frequent culprits. Acidic agents like toilet bowl cleaners, swimming pool chemicals, and battery liquids also pose significant risk. Ammonia-based products can cause both esophageal injury and chemical pneumonitis. Hair relaxers typically cause only superficial burns, while household bleach rarely results in injury due to its near-neutral pH. Industrial-strength bleach, however, may lead to more severe damage.
Acidic agents cause coagulation necrosis, limiting tissue penetration and confining injury to the superficial mucosa. Alkaline agents induce liquefaction necrosis, leading to rapid and deep transmural inflammation, edema, and a higher risk of perforation. Severity correlates with the concentration and volume of the substance ingested. Initial necrosis is followed by secondary damage due to inflammation, infection, and vascular thrombosis. Perforation risk remains elevated for approximately three weeks post-ingestion.
Children may present with a wide range of symptoms—or none at all. Dysphagia is the most common symptom, but others include vomiting, drooling, hematemesis, chest or abdominal pain, and respiratory distress. Absence of oral burns does not exclude esophageal injury.
Initial assessment includes documentation of the ingested agent’s physical form, chemical properties, and volume. Water may be used to rinse the face and mouth, but vomiting should not be induced. Neutralizing agents and activated charcoal are not recommended.
Endoscopy is generally unnecessary for asymptomatic children who ingested low-causticity substances. However, if a more caustic substance was ingested—even without symptoms—endoscopy is warranted. Symptomatic patients, those with oral burns, or those known to have ingested highly caustic substances should undergo endoscopy within 24 hours.
| Grade | Description |
|---|---|
| 0 | Normal mucosa |
| 1 | Mucosal edema and erythema |
| 2A | Superficial, noncircumferential ulcers |
| 2B | Deep focal or circumferential ulcers |
| 3A | Small scattered areas of focal necrosis |
| 3B | Extensive necrosis with brown-black or grayish discoloration |
Antibiotics and corticosteroids have unclear roles. Stricture formation is the most common long-term complication. A barium esophagram is recommended 2–3 weeks post-ingestion for injuries graded 2A or higher. Balloon dilation is preferred, though timing and frequency are not well established. Endoscopic steroid injections remain investigational.
Approximately 2% of patients with severe caustic esophageal injury may develop esophageal squamous cell carcinoma later in life.
Pill esophagitis occurs when medications lodge and dissolve in the esophagus, causing mucosal damage, ulceration, and scarring. Common offenders include tetracycline, ferrous sulfate, and phenytoin. Risk factors include inadequate water intake, esophageal dysmotility, and anatomical abnormalities. Symptoms include chest pain and dysphagia. Management involves discontinuing the medication or switching to a liquid form, initiating antireflux therapy, and considering sucralfate.
Caused by forceful vomiting or retching, resulting in linear lacerations at the gastroesophageal junction. Symptoms include hematemesis, melena, and abdominal pain. Endoscopy within 24 hours typically reveals bleeding lesions. Supportive care is usually sufficient.
Occurs when gastric mucosa prolapses through the lower esophageal sphincter during repeated emesis, causing trauma to the fundus. Presents as acute upper GI bleeding and is managed with antacids and antiemetics.
Spontaneous esophageal rupture due to a sudden rise in intraesophageal pressure, typically following vomiting. Most common site is the left posterolateral wall of the lower third of the esophagus. Symptoms include chest pain, vomiting, subcutaneous emphysema, dyspnea, cyanosis, and shock. Diagnosis is confirmed via chest X-ray, contrast esophagram, or CT scan. Treatment includes IV fluids, broad-spectrum antibiotics, and surgical repair.