OVERVIEW
Corrosive esophageal burns are mostly caused by chemical burns of the esophagus due to accidental swallowing of chemical corrosives such as strong acids or bases. Strong bases produce more severe dissolution necrosis of the esophagus; strong acids produce protein coagulation necrosis. The severity of esophageal chemical burns is determined by the type, concentration, and dosage of the chemical corrosive agent swallowed, the anatomical characteristics of the esophagus, the accompanying vomiting, and the duration of the corrosive agent’s contact with the tissue. After swallowing a chemical corrosive, the burn is often not limited to the esophagus, but often includes the oropharynx, larynx, stomach, or duodenum. Usually the corrosive agent is in contact with the three physiologic strictures of the esophagus for the longest period of time, and therefore more extensive burns often occur in these areas.
Etiology
Chemical burns of the esophagus are usually caused by accidental swallowing of chemical corrosives such as strong acids or bases. There are also due to long-term reflux esophagitis, long-term intake of concentrated vinegar or long-term use of acidic drugs (such as doxycycline, tetracycline, aspirin, etc.) caused by esophageal chemical burns, but less common. Chemical burns are less common. Thus more extensive burns often occur in these areas.
Symptoms
Immediately after accidental ingestion of a corrosive agent, severe pain is caused in the lips, mouth, pharynx, retrosternum, and epigastrium, followed by reflex vomiting, and the vomit is often bloody. If the burns involve the epiglottis, larynx and respiratory tract, coughing, hoarseness, dyspnea, and in severe cases, coma, collapse, fever and other symptoms of poisoning. Scar stenosis formation can lead to partial or complete obstruction of the esophagus, and even saliva is difficult to swallow. Due to the inability to eat, malnutrition, dehydration, emaciation, anemia, etc. occur in the later stage. In children, growth and development are affected. According to the degree of the pathology of the burn, it is graded:
1. First degree
The esophageal mucosa is superficially congested and edematous, and heals in 7-8 days after the desquamation period without scarring.
2.Ⅱ degree
The burns involve the muscular layer of the esophagus. In the acute stage, tissue congestion, edema, exudation, tissue necrosis and shedding to form an ulcer. 3-6 weeks of granulation tissue proliferation. Later, the fibrous tissue forms a scar and leads to stenosis.
3. Third degree
Coagulation and necrosis of the whole esophagus and its surrounding tissues may lead to esophageal perforation and mediastinitis.
The pathologic process after cauterization can be broadly divided into three stages. In the first stage, inflammation, edema or necrosis occurs in the first few days after the injury, and early symptoms of esophageal obstruction often appear. In the second stage, 1 to 2 weeks after injury, the necrotic tissue begins to fall off and soft, reddish granulation tissue appears, and the symptoms of obstruction are often alleviated. The esophageal wall is weakest at this time and lasts 3 to 4 weeks. In the third stage scarring and strictures form and gradually worsen. The pathologic evolution may proceed for weeks to months, but reoccurrence of stenosis after more than 1 year is rare. The favored sites of scarring and stenosis are often in the physiologic strictures of the esophagus, i.e., at the entrance of the esophagus, at the plane of the tracheal bifurcation, and at the lower end of the esophagus.
Examination
1. Medical history
A brief history is taken, including the type, time, concentration and amount of corrosive agent taken.
2. Iodized oil imaging of the esophagus
3. X-ray examination
X-ray barium meal examination of the esophagus can clarify the location and degree of stenosis.
Diagnosis
In the early stage, the diagnosis can be established mainly on the basis of the history of corrosive agent swallowing and the clinical manifestations mentioned above, and the physical examination reveals that there are burns in the oropharynx. However, sometimes the presence or absence of oropharyngeal burns does not necessarily prove the presence or absence of esophageal burns, so the diagnosis should be confirmed by esophageal iodine-oil angiography if necessary. Retrosternal pain, back or abdominal pain should exclude esophageal or gastric perforation. X-ray imaging of the esophagus in advanced stages can clarify the location and extent of the stricture.
Treatment
1. Emergency treatment procedures are as follows
(1) Take a brief history, including the type, time, concentration and amount of corrosive agent taken.
(2) Rapidly determine the patient’s general condition, especially the respiratory system and circulatory system. Keep the airway open, and tracheotomy if necessary. Establish intravenous access as soon as possible.
(3) Swallow vegetable oil or protein water as early as possible to protect the esophagus and gastric mucosa. When unconditional even swallow saline or water to dilute. Controversy exists over the previous method of neutralizing alkaline substances with weak acid solutions and alkaline solutions with acidic substances. Some believe that this method is not only unhelpful, but also harmful, because the heat generated by the chemical reaction can cause re-injury.
(4) Active management of complications, including laryngeal edema, shock, gastric perforation, and mediastinitis.
(5) Prevent esophageal stenosis, early use of adrenocorticotropic hormone and antibiotics can reduce inflammatory reaction, prevent infection, fibrous tissue proliferation and scar formation. Hormones are prohibited for those suspected of having esophageal and gastric perforation. Whether endoluminal tube is placed for esophageal luminal stent or esophageal compression method to prevent stenosis, its effect is still controversial.
2. Dilatation therapy
Dilatation therapy should be carried out after the acute inflammation and edema of the esophagus begin to subside 2 to 3 weeks after the injury. For mild annular stenosis, esophagoscopic strip dilatation can be used, and for long tubular stenosis, swallowing wire should be used to pull out through the gastrostomy port, and tighten the dilatator to dilate in the downward or reverse direction. Esophageal dilatation should be repeated at regular intervals.
3. Surgical treatment
Surgery can be used for severe long stenosis and failure of dilatation therapy. The esophagus is cut off above the stricture and replaced by anastomosis of the stomach, jejunum, or colon, as appropriate. The narrowed esophagus is left open or resected. The gastric or intestinal segment can be lifted via the pleural cavity, retrosternal or anterior sternal subcutaneous route, depending on the patient’s general condition.
Prevention
Prevent accidental swallowing of chemical corrosives such as strong acids or bases.