While accidental ingestion of caustic materials is common in children, intentional ingestion is the leading cause of caustic esophageal injury in adults. The diagnosis should be suspected in all patients brought to the emergency ward for attempted suicide. The injury may be fatal and warrants immediate treatment. Identifying the nature of the ingested substance is paramount to proper management because the severity and nature of the injury are related to the chemical and physical properties of the caustic agent (i.e., acid versus base, solid versus liquid, concentration, quantity, and duration of contact with esophageal tissues).¹ These exposures cause injuries ranging in severity from first-, second-, or third-degree burn to full-thickness necrosis and frank perforation, often requiring surgical treatment.

ANATOMY

In chemical burn injuries, the esophageal sites most susceptible are the three areas of normal anatomic narrowing (Fig. 42-1). These are the upper esophagus at the cricopharyngeus, the midesophagus where the aorta and left main stem bronchus impinge, and the distal esophagus proximal to the lower esophageal sphincter. Passage of the ingested material may be delayed through these regions, increasing the duration of exposure and potential for injury. Lower esophageal sphincter hypotension associated with reflux causes prolonged exposure of the distal esophagus to the caustic agent. This is exacerbated by pylorospasm, particularly associated with alkali ingestion, which propagates the injury by causing regurgitation of caustic contents back into the esophagus.² While there may be relative tolerance of the esophageal squamous epithelium to ingested acid, pylorospasm still may lead to pooling of acid, severe gastritis, and full-thickness necrosis with perforation.

ETIOLOGY

Acids cause coagulation necrosis, which is characterized by the formation of eschar. This deposition of dead black tissue often limits the injury to the superficial esophageal lining. Alkaline exposure causes liquefactive necrosis, which allows the caustic agent to penetrate the esophageal wall more deeply, thereby escalating the severity of the injury.³ Since the degree of injury is also associated with duration of exposure, it is important to determine whether the ingested material is a solid or a liquid. Solid alkali tends to adhere to the oropharyngeal region, whereas liquid alkali passes more quickly, causing greater esophageal and gastric injury.^4,5

The three phases of chemical injury are (1) inflammation/necrosis, (2) sloughing and ulceration, and (3) fibrosis with stricture formation. Management is guided by early flexible esophagoscopy to grade the degree of injury, usually within 24 hours of injury, after the patient has been stabilized. First-degree burn is characterized by hyperemia and edema; second-degree burn, by ulceration; and third-degree burn, by massive edema often with eschar formation with or without full-thickness necrosis, which may depend on the acid or basic nature of the ingestion.⁶ First-degree esophageal burns generally require observation alone because these injuries do not cause perforation or strictures. Second- and third-degree burns of the esophagus require ongoing monitoring for perforation or progression to generalized necrosis. Perforation or near-perforation requires immediate surgical intervention (see Chap. 40), whereas the absence of full-thickness necrosis and perforation necessitates frequent reevaluation and investigation over a prolonged time period.

ACUTE PRESENTATION

The symptoms of caustic ingestion include oral pain, drooling, inability or refusal to swallow secondary to pain, and hematemesis. Hoarseness, stridor, or dyspnea suggests a laryngeal or supralaryngeal injury. Symptoms of acute perforation include progressive neck, substernal, back, or abdominal pain. Signs of acute perforation are tachycardia, fever, subcutaneous emphysema, pericardial crunch, and chest dullness to percussion. Absence of symptoms does not entirely exclude significant injury, but the number of signs and symptoms present correlates with severity of injury.

Initial evaluation includes history and physical examination. History includes verification of the caustic agent and documentation of the time between exposure and treatment. Radiologic evaluation includes chest x-ray; esophagram; and neck, chest, and abdominal CT scans. Initial CT scans may be performed without contrast agents, although the administration of water-soluble contrast material improves the predictive value of the scan and can substitute for an esophagram when this study is unobtainable.

All caustic ingestion patients are monitored with telemetry and placed on IV fluids. Patients are kept nothing by mouth during the initial evaluation. Prophylactic IV H₂-blockers or proton pump inhibitors are administered routinely for both symptom relief and to lessen and treat reflux.⁷ Esophagogastroduodenoscopy for complete evaluation is carried out by 24 hours after injury, if possible (see Chap. 12).

CONSERVATIVE MANAGEMENT

Patients with first-degree burn are observed for at least 48 hours while their oral diet is advanced cautiously. Patients with second- or third-degree injuries without perforation should be admitted to the ICU and treated with broad-spectrum antibiotics and possibly steroids. While controversial, the administration of antibiotics and steroids may help to lessen gastrointestinal bacterial translocation and to decrease inflammation. These, in turn, may decrease the frequency and severity of stricture formation, as well as the necessity of multiple subsequent esophageal dilations. Steroid administration also may relieve airway obstruction owing to mucosal edema and bronchospasm in the acute setting.⁶ Proton pump inhibitors are used to decrease reflux secondary to impaired esophageal function at the lower esophageal sphincter, which also may increase the potential for stricture formation. Patients are monitored with serial chest x-rays. Nothing by mouth status is maintained until the patient is able to swallow saliva without pain. A means for nutrition is established. Indications of upper airway injury are managed with bronchoscopy, laryngoscopy, and possibly intubation or tracheostomy. An initial esophagram with water-soluble contrast material is obtained within 48 hours and is repeated at intervals (non-water-soluble contrast material may be used) as clinically indicated. Consideration may be given to various surgical treatments (discussed below) throughout the patient's hospital course.

Intermediate-term follow-up at 3-4 weeks, 3 months, and 6 months is necessary to monitor for stricture formation, gastric outlet obstruction, and the development of hourglass esophagus or linitis plastica.^1,8,9 Beyond 6 months, long-term follow-up is required to monitor for the development of esophageal dysmotility or esophageal squamous cell carcinoma.

SURGICAL MANAGEMENT

Surgical management of chemical and burn injuries of the esophagus includes several broad categories of procedures and operations. Initial diagnostic procedures include bronchoscopy and esophagogastroduodenoscopy. Exploratory laparotomy, esophageal stenting, and enteral feeding tube insertion or parenteral feeding access are surgical procedures used often during the initial hospitalization of a chemical burn injury patient. Surgical intervention in the acute setting is rare but may be indicated for a full-thickness injury that results in esophageal perforation or diffuse necrosis evidenced by a systemic inflammatory response. Esophageal dilation is often required during the subacute phase of chemical burn esophageal injury. Surgical resection with reconstruction may be considered in the subacute or chronic phase of injury after a severely strictured esophagus has failed multiple dilations. Resection ultimately may be required despite the type of surgery initially performed to reduce the risk of late carcinoma, which approaches 40% and manifests after a delay of 20–50 years.^10,11

The approach to the acute surgical management of chemical and burn injuries of the esophagus depends on findings during the initial survey, ongoing developments that occur during hospitalization, and the timing of those developments. Full-thickness necrosis of the esophagus employs surgical and management techniques similar to the treatment of esophageal perforation. Complete resection, whether immediate or delayed, involves techniques that are identical to those for esophagectomy in malignant disease.²

In the absence of full-thickness necrosis, corrosive injury to the esophagus is managed with surgical intervention in the setting of delayed, subacute, or isolated perforation (see Chap. 40) or for adjunct procedures such as enteral or IV access. Surgery is also indicated for the management of strictures, the timing of which is controversial.^8,12 Most often the surgical management of strictures is delayed until the injury is subacute or chronic in nature.^6,13

Esophagoscopy/Esophagogastroduodenoscopy

Esophagoscopy is used for evaluation in nearly every patient with esophageal caustic injury. However, esophagogastroduodenoscopy may be impossible to complete depending on the severity of the patient's injury. The flexible gastroscope should be advanced only as far as the first severe burn injury to establish its location and grade. Endoscopy distal to the site of first injury risks iatrogenic perforation.

Exploratory Laparotomy

Exploratory laparotomy has been reported by Estrera and colleagues as an adjunct to esophagoscopic assessment for patients with second- and third-degree burns seen on esophagoscopy. In this approach, all patients with burns and full-thickness necrosis undergo radical esophagogastrectomy, cervical esophagostomy, and feeding jejunostomy. Patients without full-thickness necrosis undergo intraluminal stent placement for 21 days to prevent obliteration of the esophageal lumen and as a scaffold to promote epithelial ingrowth. Estrera and colleagues have reported excellent results in the prevention of stricture formation using this technique, although laparotomy for grading of esophageal corrosive injuries and preemptive stenting of strictures have not gained widespread popularity.⁸

Surgery for Caustic Esophageal Full-Thickness Necrosis and Perforation

The surgical approach to esophagectomy may vary greatly among surgeons, and readers are referred to Chapters 10–23. Reconstruction generally is delayed at least 6 months because of the severe systemic derangement that follows a corrosive esophageal injury.¹ While the stomach is the reconstructive conduit of choice in most esophagectomy patients, this conduit may be unavailable owing to injury at the time of the initial insult. Reconstruction with colonic or jejunal interposition grafts may be necessary.

Despite surgical resection techniques analogous to those used for other esophageal and malignant disease, the decision to resect for chemical and burn esophageal injuries can be difficult.¹⁴ Full-thickness biopsies of the esophageal wall are not possible, and other data obtained with minimally invasive procedures such as esophagoscopy are incomplete. Changes over time in the appearance of the esophagus and the patient's clinical status are the most helpful indicators of irreversible necrosis of the esophagus. But these data are incomplete and have incumbent risk because close observation without intervention can lead to irreversible sepsis or shock and esophagoscopy carries a risk of perforation.

The surgical management of caustic esophageal perforation depends on many factors: the size and location of the perforation, the state of neighboring tissues, and the patient's overall clinical status.¹⁵ Extensive full-thickness esophageal and gastric necrosis is treated urgently with total esophagogastrectomy with diverting cervical esophagostomy. In this manner, oropharyngeal secretions are diverted from the site of the perforation.¹⁴This procedure involves resection (often transhiatal) and diversion; the details of the surgical conduct of this procedure are described in Chapters 10–23 (esophagectomy) and Chapter 40 (esophageal perforation). In the setting of extensive esophageal necrosis, exclusion and diversion generally are not an option for treatment. The necrotic esophagus in this situation leads to ongoing mediastinal soilage, systemic inflammatory response, and sepsis. It is therefore rarely left in situ once necrosis or perforation has occurred.

Surgery for Caustic Esophageal Strictures

Esophageal stricture formation is the most frequent sequela of second- or third-degree esophageal burn. Steroids have no proven benefit in the prevention of stricture formation.⁷ The time to development of strictures is variable and can occur days to as long as months after the injury. Most commonly, strictures develop between 3 weeks and 3 months after caustic ingestion, with the peak at 2 months.^9,13 Many strictures are mild to moderate in nature and will respond to dilation, often without recurrence. These strictures can be dilated using the standard methods (e.g., Savary, bougienage, or pneumatic) described in detail in Chapter 36.

Other strictures that occur after caustic esophageal exposure present a greater therapeutic challenge. These are often very tight, long, and thick-walled; they can occur in series, which are very difficult to dilate and recur quickly. Since there is no single uniformly effective treatment, many strategies have been suggested and are practiced. One strategy to prevent these strictures involves early bougienage, with treatment performed daily for several weeks before being liberalized to every other day for several weeks and then weekly for months. This practice has not been proved to eliminate strictures but may lead to earlier resolution of strictures, although the incidence of perforation and associated morbidity is high. Many surgeons, however, do not perform esophageal dilations until 3–6 weeks after injury. Long (>1.5 cm) and eccentric strictures require dilation under fluoroscopic guidance.⁶ An in-situ tube (e.g., Dobhoff, nasogastric, or string or bead chain) provides a path through the esophageal stricture(s) and allows for dilation of tight strictures by preventing complete esophageal luminal obliteration. A nasogastric string or stainless steel bead chain, along with a gastrostomy tube, may facilitate retrograde dilation of strictures and is used commonly in pediatric patients. Local injection of corticosteroids via gastroscopy and followed by bougienage also can be a useful strategy for managing recalcitrant postcaustic injury esophageal strictures.¹ Another strategy, mentioned previously, is placement of self-expanding intraluminal stents. Stents have found limited success and may not be applicable for severe strictures, except as a temporizing measure.¹²

Elective esophagectomy with colon interposition may be required for treatment of severe strictures after caustic ingestion. The use of a gastric tube replacement conduit for severe stricture may be an option in selected patients. Rarely, the severity of initial injury associated with caustic ingestion causes obliteration of the esophagus with mediastinal fibrosis, necessitating passage of the conduit (e.g., colon, stomach) through an alternate route (i.e., subcutaneous, retrosternal, transthoracic). Details regarding these operative techniques can be found in the chapters in Part 2 as well as in Chapter 38. Similarly, esophageal bypass, leaving the scarred esophagus in situ, has been described. Unfortunately, continued monitoring for the development of esophageal carcinoma is difficult in this scenario. Additionally, the development of esophageal mucoceles has been reported within the retained esophageal segment.^16,17

Esophageal Bypass

Esophageal bypass is an uncommon but valuable thoracic surgical operation that is performed most often in patients with benign or malignant strictures of the esophagus, unresectable esophageal cancer, esophageal perforation, and malignant or congenital tracheoesophageal fistula. Variations in surgical technique abound, but the result of surgery is orointestinal continuity and a bypassed esophagus that is excluded from the gastrointestinal system at the proximal end or sometimes at both ends. A gastric conduit or colon conduit is used most commonly for the bypassed esophagus.^18,19

Preoperatively, the patient undergoes bowel preparation via an in-situ feeding tube, if applicable. Perioperative antibiotics are administered. The patient is placed in the supine position with modest neck extension, and the neck, chest, and abdomen are prepped and draped in the usual sterile fashion. A collar incision 1 cm above the suprasternal notch is extended leftward and parallel to the anterior border of the sternocleidomastoid muscle to access the deep cervical space (Fig. 42-2). The omohyoid and other strap muscles are divided as needed, and the carotid sheath and jugular vein are retracted laterally. Blunt dissection is used to mobilize the posterior esophageal wall from the lower cervical vertebrae (Fig. 42-3). A bougie dilator, gastroscope, or tube inserted in the proximal esophagus may guide identification of the proximal esophagus. Once the trachea is separated from the anterior esophageal wall using scissors or blunt dissection, the esophagus is encircled. Transection of the esophagus is performed using a linear stapler. The distal cervical esophagus is permitted to retract into the mediastinum. A drain is inserted in the area (Fig. 42-4).

A midline laparotomy incision is used to access the abdomen. Preparation of the conduit (i.e., stomach or colon) for bypass is analogous to conduit creation for esophageal reconstruction after esophagectomy, with minor differences. If the esophagus is obliterated into the gastroesophageal junction, this can be divided using a linear stapler. If this is patent and the stomach is to be used for a conduit, the stomach is divided from the top of the fundus to a point between branches of the right and left gastric vessels on the lesser curvature (Fig. 42-5). The left gastric vessels are preserved for blood supply to the cardia. This excluded part can be drained with a tube, via jejunal anastomosis (Roux-en-Y), or fistulized externally to the abdominal wall as a cardiostomy.²⁰

A subcutaneous or substernal tunnel is created bluntly between the two skin incisions. The conduit is brought to the neck, and a cervical anastomosis is created. Gastrointestinal continuity using a colon conduit is reestablished with cologastric or colointestinal anastomosis (Fig. 42-6). Details of these aspects of the procedure are described in Part 2 of this text.

Esophageal bypass has only modest utility in the treatment of esophageal caustic injury. In most cases the native esophagus should be removed, if possible, because of the long-term risk of developing esophageal cancer in the injured esophagus.^10,11 Nonanatomic esophageal reconstruction is suboptimal and is avoided if appropriate and technically feasible. Mucocele formation in the retained esophageal remnant is a theoretical complication of esophageal bypass for caustic esophageal injury. Mucoceles may form in the excluded esophageal segment but usually are small and asymptomatic.¹⁶ As a result of mucosal obliteration and fibrosis from caustic injury, mucoceles are less likely to form in this setting than in the case of bypassed esophageal segments owing to other benign or malignant esophageal diseases.

SUMMARY

Surgical management of injury from ingested caustic agents varies depending on the exact nature of the injury and the patient's clinical course (Fig. 42-7). Nearly all patients require esophagoscopy. Adjunct procedures may be required. Surgery in the acute setting of extensive esophageal or gastric necrosis with perforation requires surgical resection and diversion. Esophageal exclusion or bypass is an option in selected patients with subacute or isolated perforations. Reconstructive surgery is always delayed but is technically analogous to reconstruction in other esophageal diseases. Strictures after caustic esophageal injury are exceedingly common. In the long term, esophageal resection is often required eventually for functional failure of the native esophagus or for management of esophageal cancer, which develops in survivors.

EDITOR'S COMMENT

Caustic esophageal injuries are often self-inflicted. For these cases, the thoracic surgeon must assemble a team including family members and psychiatrists both to prevent further suicide attempts and to optimize the psychological condition of the patient during the prolonged treatment course.

–RB

REFERENCES