50: Surgical Management of Corrosive Injury to the Esophagus

While accidental ingestion of caustic materials is more 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 vs. base, solid vs. 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.

In chemical burn injuries, the esophageal sites most susceptible are the three areas of normal anatomic narrowing (Fig. 50-1). These are the upper esophagus at the cricopharyngeus, the midesophagus where the aortic arch and left mainstem bronchus cross, and the distal esophagus proximal to the lower esophageal sphincter (LES). Passage of the ingested material is delayed through these regions, increasing the duration of exposure and potential for injury. Reflux-associated LES hypotension 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 Although there may be relative tolerance of the esophageal squamous epithelium to ingested acid, pylorospasm may lead to pooling of acid, severe gastritis, and full-thickness necrosis with perforation.

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 and location of injury. Chemical burns are graded according to Zargar's 6-point classification of caustic mucosal injury as assessed from endoscopy.⁶ First-degree burn (Grade 1) is characterized by hyperemia and edema; second-degree burn (Grade 2A, 2B), by ulceration; and third-degree burn (Grade 3A, 3B), by black or gray discoloration indicative of necrosis.⁷ 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 Chapter 48), whereas the absence of full-thickness necrosis and perforation necessitates frequent reevaluation and investigation over a prolonged time period.

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. Airway management is of paramount importance because of possible associated burns to the larynx. Intubation guided by fiberoptic or rigid bronchoscopy should be performed. One should be prepared to perform a surgical airway if required. After the airway is addressed, a thorough history and physical examination is completed. History includes verification of the caustic agent and documentation of the time between exposure and treatment. 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.

Radiologic evaluation may include chest x-ray and CT scans to rule out pneumomediastinum or free intraperitoneal air. Initial CT scans of the neck, chest, and abdomen may be performed without contrast agents, although the administration of water-soluble contrast material improves the predictive value of the scans. Barium esophagram is of limited utility in the initial evaluation as it carries a 30% to 60% false-negative rate.⁸

All caustic ingestion patients are monitored with telemetry and resuscitated with IV fluids. Patients are kept nothing by mouth and given prophylactic IV H₂-blockers or proton pump inhibitors for both symptom relief and to treat reflux.⁹ Flexible esophagoscopy is used for evaluation in nearly every patient with esophageal caustic injury. There is controversy regarding the optimal timing for initial endoscopic evaluation.¹⁰ In the past, there was a tendency to wait at least 24 hours of injury, after the patient had been medically stabilized. Most agree that flexible esophagogastroduodenoscopy for complete evaluation should be carried out between 12 and 24 hours after injury (see Chapter 14). Endoscopy past 48 hours is discouraged due to the increased risk of perforation attributable to progressive wall weakening. Esophagogastroduodenoscopy may be impossible to complete depending on the severity of the patient's injury. The flexible scope may be carefully advanced past a site of mild injury but should be stopped at the site of circumferential Grade 2 and 3 injuries. Endoscopy distal to the site of first injury risks iatrogenic perforation.

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, respectively.^11-13 This may decrease the frequency and severity of stricture formation, as well as the necessity of multiple subsequent esophageal dilations, although the side effects of steroids with regard to increased susceptibility to infection should be carefully considered. Steroid administration also may relieve airway obstruction owing to mucosal edema and bronchospasm in the acute setting.⁷ Reflux secondary to impaired esophageal function at the LES may also increase the potential for stricture formation. Proton pump inhibitors are employed to reduce reflux. Patients are monitored with serial chest x-rays. NPO status is maintained until the patient is able to swallow saliva without pain. A means for either enteral or parenteral nutrition is established. Rigid endoscopy is recommended for the safe placement of nasogastric tube, which serves both to stent the area of injury as well as to provide enteral nutrition. An initial esophagram with water-soluble contrast material is obtained within 48 hours and may be repeated at intervals 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 to 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.^1,10,14 After 6 months, long-term follow-up is required to monitor for the development of esophageal dysmotility or esophageal squamous cell carcinoma.

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. Surgical techniques employed in this setting include esophageal resection and diversion, as is applied in severe cases of necrotizing esophageal perforation (see Chapters 48, 51, and 58).

In the subacute phase, esophageal dilation is often required for the treatment of strictures. Surgical resection with reconstruction may be considered in the chronic phase of injury after a severely strictured esophagus has failed repeated dilations. Esophagectomy ultimately may be required to reduce the risk of late carcinoma, which approaches 40% and manifests after a delay of 20 to 50 years.^15,16

Exploratory Laparotomy

Exploratory laparotomy has been reported by Estrera and colleagues as an adjunct to esophagoscopic assessment for patients with Grade 2 and 3 injuries 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.¹⁰

Surgical Resection for Caustic Esophageal Full-Thickness Necrosis and Perforation

The surgical approach to esophagectomy may vary greatly among surgeons, and readers are referred to Chapters 13 to 27. Reconstruction generally is delayed at least 6 months because of the severe systemic derangement that follows a corrosive esophageal injury.¹ Although 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.

Although the techniques of surgical resection are analogous to those used for malignant esophageal disease, the decision to resect for chemical burn-associated esophageal injuries can be more challenging.¹⁷ Full-thickness biopsies of the esophageal wall are not possible, and other data obtained with procedures such as esophagoscopy are incomplete. Changes over time in the endoscopic or radiographic appearance of the esophagus and the patient's clinical status are the most helpful indicators of irreversible necrosis of the esophagus.

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.¹⁸ 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.¹⁷ This procedure involves resection (often transhiatal) and diversion; the details of the surgical conduct of this procedure are described in several esophagectomy technique chapters in Part 2 and in Chapter 48 on esophageal perforation. In the setting of extensive esophageal necrosis, diversion without resection is not an option for definitive 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.

The critically ill status of the patient requiring esophageal resection for necrotizing corrosive injury precludes esophageal reconstruction in the acute setting. After the patient has been clinically stabilized, esophageal replacement may be electively planned.

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.⁹ 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.^14,19 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 44.

Other strictures that occur after caustic esophageal exposure present a greater therapeutic challenge, making it difficult to dilate, and can 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 decreased 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 to 6 weeks after injury. Long (>1.5 cm) and eccentric strictures require dilation under fluoroscopic guidance.⁷ An in-situ tube (e.g., Dobhoff, nasogastric, or string or bead chain) provides a guide 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 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.²⁰ Some may advocate placement of stents to avoid repeated dilations. Apart from case series, there are no studies to validate schedules for dilation of caustic strictures, or to guide management of caustic strictures with stents.

For the definitive treatment of refractory caustic strictures, elective esophagectomy with reconstruction may be indicated. 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 51.

Esophageal Bypass

Esophageal bypass is performed 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 left in situ that is excluded from the gastrointestinal system at both ends. A gastric or colon conduit is used most commonly for the bypassed esophagus.^21,22 In recent years, the use of esophageal bypass particularly in the setting of malignant esophageal disease has been replaced by the widespread use of esophageal stents. However it remains a valuable technique to maintain within one's armamentarium.

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. 50-2). 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. 50-3). A bougie dilator, gastroscope, or tube inserted in the proximal esophagus may guide identification of the proximal esophagus. The esophagus is encircled once the anterior esophageal wall is carefully separated from the trachea using sharp dissection. Caution is taken to not injure the posterior membranous wall of the trachea or the recurrent laryngeal nerve on either side. Transection of the esophagus is performed using a linear stapler. Now divided, the distal cervical esophagus is permitted to retract into the mediastinum. A drain is inserted in the area (Fig. 50-4).

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. 50-5). 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.²³

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. 50-6). 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.^15,16 Continued monitoring for the development of esophageal carcinoma is difficult once the native esophagus has been bypassed. Nonanatomic esophageal reconstruction is suboptimal and is avoided if possible. 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.^24,25 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 due to other benign or malignant esophageal diseases.

Surgical management of injury from ingested caustic agents varies depending on the exact nature of the injury and the patient's clinical course (Fig. 50-7). Prompt recognition of the process and aggressive treatment to resuscitate the patient is essential. Nearly all patients require esophagoscopy. Adjunct procedures may be required. Surgery in the acute setting of extensive esophageal and/or gastric necrosis with perforation requires resection and diversion. Reconstruction or bypass may be considered in the elective setting once the patient has been clinically stabilized. Esophageal bypass alone is rarely employed, as resection of the native esophagus is recommended due to the risk of malignant degeneration and of mucocele formation in the retained esophageal segment. Reconstructive surgery is technically analogous to reconstruction after esophagectomy, except that a nongastric conduit may be required. Strictures after caustic esophageal injury are exceedingly common and may be initially managed with serial dilation. In the long term, esophageal resection is often required for refractory strictures with functional failure of the native esophagus or for management of esophageal cancer, which develops in survivors.

Corrosive injuries of the esophagus used to be commonplace in the 1960s, 70s, and 80s, when numerous poisons were kept within most American homes. As homes and product containers have become increasingly child-proofed, corrosive injuries have become rare. This chapter provides straightforward information in a readily accessible manner for the reader who may be called upon to manage their first corrosive esophageal injury. These are life-threatening burns to the esophagus and must be quickly managed to prevent esophageal perforation or extensive organ necrosis. One important take away message is that it is safer to perform endoscopy to characterize the extent of esophageal injury within the first 12 hours than 48 hours later when there is more edema in the esophageal wall. Stents to open and manage strictures have been a major advance in this disease. Postinjury strictures can be very long and extremely resistant to dilation, leading to esophagectomy. Early stenting may save the organ and produce a better long-term functional result.