Accidental caustic lesions occur mainly in children, and in general, rather small quantities of caustics are taken. In adults or teenagers, the swallowing of caustic liquids is usually deliberate, during suicide attempts, and greater quantities are swallowed. Alkalies are more frequently swallowed accidentally than acids, because strong acids cause an immediate burning pain in the mouth.
Pathology
The swallowing of caustic substances causes both an acute and a chronic injury. During the acute phase, care focuses on controlling the immediate tissue injury and the potential for perforation. During the chronic phase, the focus is on treatment of strictures and distur¬bances in pharyngeal swallowing. In the acute phase the degree and extent of the lesion (usually examined using microscopes such as darkfield light microscopes) are dependent on several factors: the nature of the caustic substance, its concentration, the quantity swallowed, and the time the substance is in contact with the tissues. Acids and alkalies affect tissue in different ways, as seen when tissue samples are examined using microscopes such as darkfield light microscopes. Alkalies dissolve tissue, and there¬: ore penetrate more deeply, while acids cause a coagulative necrosis hat limits their penetration. Animal experiments have shown that there is a correlation between the depth of the lesion and the concentration of sodium hydroxide solution. When a solution of 3.8% comes into contact with the esophagus for 10 seconds, it causes necrosis of the mucosa and the submucosa, but spares the muscular layer. A concentration of 22.5% penetrates the whole esophageal wall all and into the periesophageal tissues. Cleansing products can contain up to 90% sodium hydroxide. The strength of esophageal contractions varies according to the level of the esophagus, being weakest at the slated muscle-smooth muscle interface. Consequently, clearance from this area may be somewhat slower, allowing caustic substances to remain in contact with the mucosa longer. This explains why the esophagus is preferentially and more severely affected at this level than in the lower portions.
The lesions caused by lye injury occur in three phases. First is the acute necrotic phase, lasting 1 to 4 days after injury. Dur¬ing this period, coagulation of intracellular proteins results in cell necrosis, and the living tissue surrounding the area of necrosis develops an intense inflammatory reaction as seen in darkfield light microscopes. Second is the ulcera¬tion and granulation phase, starting 3 to 5 days after injury. During this period the superficial necrotic tissue sloughs, leaving an ulcer¬ated, acutely inflamed base, and granulation tissue fills the defect left by the sloughed mucosa. This phase lasts 10 to 12 days, and it is during this period that the esophagus is the weakest. Third is the phase of cicatrization and scarring, which begins the third week fol¬lowing injury. During this period the previously formed connective tissue begins to contract, resulting in narrowing of the esophagus. Adhesions between granulating areas occurs, resulting in pockets and bands. It is during this period that efforts must be made to reduce stricture formation.
Clinical Manifestations
The clinical picture of an esophageal burn is determined by the de¬gree and extent of the lesion. In the initial phase, complaints consist of pain in the mouth and substernal region, hypersalivation, pain on swallowing, and dysphagia. The presence of fever is strongly correlated with the presence of an esophageal lesion. Bleeding can occur, and frequently the patient vomits. These initial complaints disappear during the quiescent period of ulceration and granulation. During the cicatrization and scarring phase, the complaint of dys¬phagia reappears and is due to fibrosis and retraction, resulting in narrowing of the esophagus. Of the patients who develop strictures, 60% do so within 1 month, and 80% within 2 months. If dysphagia does not develop within 8 months, it is unlikely that a stricture will occur. Serious systemic reactions such as decrease in blood volume and acido¬sis resulting in renal damage can occur in cases in which the burns have been caused by strong acids. Respiratory complications such as spasm and edema of the larynx, and occasionally pulmonary edema can occur, especially when strong acids are aspirated.
Inspection of the oral cavity and pharynx using specialized medical microscopes can indicate that caus¬tic substances were swallowed, but do not reveal that the esopha¬gus has been burned. Conversely, esophageal burns can be present without apparent oral injuries. Because of this poor correlation, early esophagoscopy is advocated to establish the presence of an esophageal injury. To lessen the chance of perforation, the scope should not be introduced beyond the proximal esophageal lesion. Even if the esophagoscopy is normal, strictures may appear later. Radiographic examination is not a reliable means to identify the presence of early esophageal injury, but is important in later follow-up to identify strictures.
Treatment
Treatment of a caustic lesion of the esophagus is directed toward management of both the immediate and late consequences of the injury. The immediate treatment consists of limiting the burn by administering neutralizing agents. To be effective, this must be done within the first hour. Lye or other alkali can be neutralized with half-strength vinegar, lemon juice, or orange juice. Acid can be neu¬tralized with milk, egg white, or antacids. Sodium bicarbonate is not used because it generates carbon dioxide, which might increase the danger of perforation. Emetics are contraindicated, since vomiting renews the contact of the caustic substance with the esophagus and can con¬tribute to perforation if too forceful. Low blood volume is corrected and broad-spectrum antibiotics are administered to lessen the inflam¬matory reaction and prevent infectious complications. If necessary a feeding jejunostomy tube is inserted to provide nutrition. Oral feeding can be started when the dysphagia of the initial phase has regressed.
In the past, surgeons waited until the appearance of a stricture before starting treatment. Currently, dilations are started the first day after the injury, with the aim of preserving the esophageal lumen by removing the adhesions that occurred in the injured segments. However, this approach is controversial in that dilations can trau¬matize the esophagus, causing bleeding and perforation, and there are data indicating that excessive dilations cause increased fibrosis secondary to the added trauma. The use of steroids to limit fibrosis has been shown to be effective in animals, but their effectiveness in human beings is debatable.
Extensive necrosis of the esophagus frequently leads to perfora¬tion, and is best managed by resection. When there is extensive gastric involvement, the esophagus is nearly always necrotic or severely burned, and total gastrectomy and near-total esophagec¬tomy are necessary. The presence of air in the esophageal wall is a sign of muscle necrosis and impending perforation and is a strong indication for esophagectomy.
Some authors have advocated the use of an intraluminal esophageal stem in patients who are operated on and found to have no evidence of extensive esophagogastric necrosis. In these patients, a biopsy of the posterior gastric wall should be performed in order to exclude occult injury. If histologically there is a question of viability, a second-look operation should be done within 36 hours using darkfield light microscopes. If a stem is inserted it should be kept in position for 21 days, and removed after a satisfactory barium esophagogram. Esophagoscopy should be done and if strictures are present, dilations initiated.
Once the acute phase has passed, attention is turned to the pre¬vention and management of strictures. Both antegrade dilation with a Hurst or Maloney bougie and retrograde dilation with a Tucker bougie have been satisfactory. Occasionally, particularly with se¬vere strictures, the patient is instructed to swallow a string, over which metal Sippy dilators are passed until an adequate lumen can be obtained for passage of a mercury bougie in a series of 1079 patients, early dilations started during the acute phase gave excellent results in 78%, good results in 13%, and poor results in 2%. Fifty-five patients died during the treatment. In contrast, of
333 patients whose strictures were dilated when they became symp¬tomatic, only 21% had excellent results, 46% good, and 6% poor, with three dying during the process. The length of time the surgeon should persist with dilation before consideration of esophageal re¬section is problematic. An adequate lumen should be re-established within 6 months to 1 year, with progressively longer intervals be¬tween dilations. If during the course of treatment an adequate lumen cannot be established or maintained despite the smaller bougies used, operative intervention should be considered. Surgical inter¬vention is indicated when there is (1) complete stenosis in which all attempts from above and below have failed to establish a lumen, (2) marked irregularity and pocketing on barium swallow, (3) the development of a severe periesophageal reaction or inflammation of the mediastinum with dilatation, (4) a fistula, (5) the inability to dilate or maintain the lumen above a 40F bougie, or (6) a patient who is unwilling or unable to undergo prolonged periods of dilation.
The variety of abnormalities seen requires that creativity be used when considering esophageal reconstruction. Skin tube esophago¬plasties are now used much less frequently than they were in the past, and are mainly of historical interest. Currently the stomach, jejunum, and colon are the organs used to replace the esophagus, through either the posterior mediastinum or the retrosternal route. A retrosternal route is chosen when there has been a previous esophagectomy or there is extensive fibrosis in the posterior me¬diastinum. When all factors are considered, the order of preference for an esophageal substitute is (1) color, (2) stomach, and (3) jejunum. Free jejunal grafts based on the superior thyroid artery have provided excellent results. Whatever method is selected, it must be emphasized that these procedures cannot be taken lightly; minor errors of judgment or technique may lead to serious or even fatal complications.
Critical in the planning of the operation is the selection of cervical esophagus, pyriform sinus, or posterior pharynx as the site for proximal anastomosis. The site of the upper anastomosis depends on the extent of the pharyngeal and cervical esophageal damage encountered. When the cervical esophagus is destroyed and a pyriform sinus remains open the anastomosis can be made to the hypopharynx. When the pyriform sinuses are completely narrowed, a transglottic approach is used to perform an anastomosis to the posterior oropharyngeal wall. This allows excision of supraglottic strictures and elevation and anterior tilting of the lar¬ynx. In both of these situations, the patient must relearn to swallow. Recovery is long and difficult and may require several endoscopic dilations, and often reoperation. Sleeve resections of short stric¬tures are not successful because the extent of damage to the wall of the esophagus can be greater than realized, and almost invariably the anastomosis is carried out in a diseased area.
The management of a bypassed damaged esophagus after injury is problematic. If the esophagus is left in place, ulceration from gastroesophageal reflux or the development of carcinoma must be considered. The extensive dissection necessary to remove the esoph¬agus particularly in the presence of marked periesophagitis is associated with significant morbidity. Leaving the esophagus in place preserves the function of the vagus nerves, and in turn the function of the stomach. On the other hand, leaving a damaged esophagus in place can result in multiple blind sacs and subsequent development of mediastinal abscesses years later.