Corrosive esophageal burns, also known as erosive burns of the esophagus, are typically caused by the accidental ingestion of strong acids or alkalis, which lead to chemical injuries to the esophagus. Strong alkalis generally result in liquefactive necrosis, whereas strong acids typically cause coagulative necrosis.
Pathology
The severity of chemical burns to the esophagus depends on the type, concentration, and amount of the corrosive agent ingested, the anatomical characteristics of the esophagus, the presence of vomiting, and the duration of contact between the corrosive substance and the tissues.
Following the ingestion of corrosive agents, the injured areas are usually not limited to the esophagus but may also include the oral cavity, pharynx, larynx, stomach, or duodenum. The esophagus, particularly its three physiological narrowings, tends to be exposed to corrosive agents for a longer period, resulting in extensive burns in these regions.
Based on pathological severity, esophageal burns are classified into the following degrees:
- Grade I: Superficial mucosal hyperemia and edema in the esophagus, which usually heal within 7–8 days after the desquamation phase without the formation of scars.
- Grade II: Injuries involving the muscular layers of the esophagus. During the acute phase, the tissues show hyperemia, edema, and exudation. After necrotic tissue sloughs off, ulcers develop, accompanied by granulation tissue proliferation within 3–6 weeks. Subsequently, fibrous tissue forms scars, leading to strictures.
- Grade III: Coagulative necrosis affecting the entire thickness of the esophagus and surrounding tissues, which may result in esophageal perforation and mediastinitis.
The pathological process of corrosive burns can be divided into three stages:
- The initial stage, during the first few days after injury, is marked by inflammation, edema, and necrosis. Early symptoms of esophageal obstruction may develop.
- The intermediate stage, occurring 1–2 weeks after injury, is characterized by the sloughing of necrotic tissue and the emergence of soft, reddish granulation tissue. Obstruction symptoms may temporarily improve during this stage. At this time, the esophageal wall is particularly fragile, a condition that may persist for 3–4 weeks.
- The late stage is when scar tissue and strictures develop and progressively worsen. This pathological evolution may last for weeks to months, but further narrowing of the esophagus beyond one year is uncommon. Scars and strictures are more likely to occur in the physiological narrowing sites of the esophagus.
Clinical Manifestations
After ingesting a corrosive agent, patients typically experience immediate intense pain in the lips, oral cavity, pharynx, retrosternal region, and upper abdomen, often followed by reflex vomiting with blood-stained vomitus. If the burns involve the epiglottis, larynx, or respiratory tract, symptoms such as coughing, hoarseness, and dyspnea may occur. Severe cases can present with symptoms of systemic toxicity, including coma, collapse, fever, and shock. In the later stage, scar formation and strictures can lead to partial or complete esophageal obstruction. As swallowing becomes impossible, patients may develop malnutrition, dehydration, emaciation, and anemia. In children, growth and development may also be adversely affected.
Diagnosis
A diagnosis can be established based on a history of corrosive agent ingestion, related clinical symptoms, and physical findings of burns in the oral or pharyngeal region. For cases where oral and pharyngeal burns are absent but esophageal injury is strongly suspected, esophagography may be used for confirmation. For patients presenting with retrosternal pain, back pain, or abdominal pain, esophageal or gastric perforation should be ruled out. Late-stage esophagography can help determine the location and extent of strictures.
Treatment
Emergency Management
Gathering the medical history involves identifying the type, time of ingestion, concentration, and quantity of the corrosive agent.
Assessing the patient's general condition includes evaluating respiratory and circulatory system status. Maintenance of airway patency may require tracheotomy under specific circumstances, along with the establishment of intravenous access.
The ingestion of edible oil or protein solution at the earliest stage serves to protect the esophageal and gastric mucosa. In the absence of these, physiological saline or plain water may be used for dilution purposes. Acid-base neutralization methods are used cautiously due to the risk of secondary injury.
Complication management involves addressing issues such as laryngeal edema, shock, gastric perforation, and mediastinitis.
Preventing esophageal stricture during the early stage is achieved through corticosteroids and antibiotics to reduce inflammatory reactions, prevent infection, and slow fibrous tissue proliferation and scar formation. Corticosteroids are avoided in suspected cases of esophageal or gastric perforation. Decisions on whether to use esophageal stents or esophageal pressurization methods to prevent stricture remain controversial.
Dilation Therapy
Esophageal dilation therapy can be performed beginning 2–3 weeks after injury, once acute inflammation and edema have subsided. Regular and repeated dilation procedures may be required.
Surgical Management
Surgical intervention may be necessary for cases of severe extensive strictures or failure of dilation therapy. Surgery typically involves leaving the affected esophageal segment in situ or resecting it, with esophageal replacement using the stomach, jejunum, or colon. Replacement routes may involve the thoracic cavity, retrosternal space, or subcutaneous pathways.