General Thoracic Surgery (General Thoracic Surgery (Shields)) [2 VOLUME SET]
Editors: Shields, Thomas W.; LoCicero, Joseph; Ponn, Ronald B.; Rusch, Valerie W.
Title: General Thoracic Surgery, 6th Edition
Copyright 2005 Lippincott Williams & Wilkins
> Table of Contents > Volume II > The Esophagus > Section XXIII - Benign Esophageal Disease > Chapter 146 - Benign Strictures of the Esophagus
Chapter 146
Benign Strictures of the Esophagus
K. Jeyasingham
A stricture of the esophagus is a narrowing of the organ produced by pathologic change in the wall of the esophagus. By virtue of its location and its effects on the nutritional status of the individual, no stricture of the esophagus may be construed as entirely benign in its behavior. To distinguish those afflictions of the organ that cause narrowing of the esophagus without being involved in a malignant or benign neoplastic pathology, however, the term benign stricture of the esophagus is used to cover a variety of conditions. The majority of benign strictures encountered by the clinician vary according to the type of practice and population catered to by that individual. The greater proportion of strictures dealt with by a thoracic surgeon are bound to be related to malignant disease. For those situations in which an esophageal surgeon offers a service in conjunction with a gastroenterologist, however, a considerable proportion of the strictures encountered are benign and are reflux related (Table 146-1).
CONGENITAL WEBS
The only true congenital strictures are the imperforate and perforate webs. These developmental defects result from failure of canalization of the foregut tube and occur at any level, but commonly in the midesophageal region. Those strictures that occur in relation to surgery for tracheoesophageal fistula and those after gastroesophageal reflux associated with congenital hiatal herniation are, in fact, acquired strictures.
Imperforate Webs
A newborn infant with an imperforate web in the esophagus presents the same clinical picture as is noted with a type II tracheoesophageal fistula, with regurgitation of food and cyanotic episodes related to aspiration of pharyngoesophageal secretions. Diagnosis is made by failure to pass a catheter through the esophagus into the stomach and by radiologic demonstration of obstruction of 1 to 2 mL of a water-soluble radiopaque material introduced into the upper esophagus using the catheter, ensuring that the material is sucked out at the end of the examination. Because an imperforate midesophageal web is indistinguishable diagnostically from a type II tracheoesophageal fistula, the correct treatment program should be the same as that adopted for the latter condition. The danger associated with blind perforation and bougienage is best avoided by standard exploration after temporary esophagostomy and abdominal feeding gastrostomy.
Perforate Webs
The presence of a diaphragm with a passage through into the stomach, as demonstrated by contrast radiography, enables endoscopic bougienage and intermittent dilation of perforate webs under direct vision. Perforate webs may not cause symptoms immediately after birth because the thin feedings often go through the diaphragm until the consistency is changed from liquid to solid foods. The presentation may even be delayed into adolescence or early adult life, but a careful clinical history ensures a diagnosis of a congenital etiology.
Acquired Webs
Acquired webs occur at all levels of the esophagus and are more common in older age groups. They do not obstruct the lumen of the esophagus completely and may have a concentric or eccentric opening. Although the diagnosis is made with contrast-enhanced radiologic studies, the patient may present with a variety of symptoms, such as dysphagia of slow onset, regurgitation, anemia, dyspepsia, and heartburn. The location of the web is often related to the etiology of the webbing process.
Table 146-1. Classification of Benign Strictures of the Esophagus | |
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Upper Esophageal Webs
Upper esophageal webs may or may not be associated with anemia. In the syndrome described by Plummer and by Vinson (1922), Patterson (1919), and Kelly (1919), the anemia is of the iron deficiency type (i.e., hypochromic microcytic) and is associated with atrophic mucosa in the oropharynx, koilonychia, and gastric achlorhydria. The webs are eccentric and are located in the upper esophagus. The diagnosis is made with contrast radiography and is confirmed with esophagoscopy. The esophagoscopy is often also therapeutic in itself by causing the web to tear. Occasionally, the web requires avulsion with the forceps introduced through the esophagoscope. This syndrome is said to predispose to postcricoid carcinoma, although the incidence of postcricoid carcinoma noted in patients during follow-up is not known. Howard (1989) reports a probable incidence of Plummer-Vinson syndrome of 9% in women having an operation for postcricoid carcinoma. It is also observed that Plummer-Vinson syndrome, upper esophageal webs, and postcricoid carcinoma are all more common in women than in men, as noted by Shamma'a and Benedict (1958) and Howard (1989). Upper esophageal webs do occur in patients with anemia and often are associated with hyperkeratosis and alcoholism. Gastard and colleagues (1989) reported they are often considered precancerous.
Middle-Third Esophageal Webs
Middle-third esophageal webs are probably hyperkeratotic in etiology, but when a patient presents with a perforate web in the middle one-third of the esophagus, the probability of this lesion being an as yet undiagnosed congenital perforate web should be considered seriously. Such lesions also may occur as the result of surgery in the neonatal period that resulted in damage to the esophageal wall at the time of intervention, as, for example, for the repair of a tracheoesophageal fistula or atresia.
Lower-Third Esophageal Webs
Hyperkeratotic webs do develop rarely in the lower esophagus and are not associated with iron deficiency anemia unless the latter is the result of reflux esophagitis. These hyperkeratotic lesions are considered precancerous and require close surveillance.
Lower Esophageal Rings
The so-called lower esophageal rings require special mention. With most medical eponymous terms, the original descriptions of phenomena rarely bear any resemblance to subsequent adoptions of such terms. Barrett's esophagus and Schatzki's rings are good examples of such terms used in everyday esophagology. In the original description of the lower esophageal ring, Schatzki and Gary in 1953 described a radiologic appearance in some patients with lower esophageal dysphagia. Subsequent interpreters have endeavored to attribute a pathophysiologic explanation to these lower esophageal rings. Schatzki himself in 1963, having studied several such patients, concluded that the
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ring was an area of restricted distensibility rather than one of abnormal contraction, and that it occurred at the junction of the squamous and columnar linings of the mucosa. Other authors have come to similar conclusions, and it is now generally agreed that the ring of limited distensibility at the exact lower limit of the squamous mucosa is lined by squamous epithelium superiorly and columnar epithelium inferiorly. Histologic examination of tissues excised from this zone reveals chronic inflammatory cellular infiltration of the submucosa with little change in the overlying mucosa or in the underlying muscular layers.One finding remains, however: a common radiologic occurrence of a ring of persistent contraction in the lower esophagus a few centimeters above the squamocolumnar junction is associated with gastroesophageal reflux and a small hiatal herniation (Fig. 146-1). Manometric studies by Migliore and the author demonstrated a ring of high pressure distinct from the lower esophageal sphincter zone and situated a few centimeters above it. Such lower esophageal rings are associated with pain as a predominant symptom. At endoscopy under sedation, inspection with the flexible instrument often reveals an area of sustained ringlike contraction that permits the passage of the instrument but is no longer discernible when inspected using the rigid esophagoscope and general anesthesia. With these incontrovertible facts, one has to agree with Goyal and associates (1971) that two different types of lower esophageal rings exist or that the lower esophageal ring has two components.
Fig. 146-1. A barium radiographic study shows the typical appearance of a lower esophageal ring as described by Schatzki. A hiatal hernia is inevitably associated, as seen in this illustration. |
Although most published data suggest that reflux esophagitis is not the cause of Schatzki's ring, considerable evidence suggests that lower esophageal rings, reflux, and hiatal herniation are closely linked. Reflux of gastric contents is known to stimulate the lower esophagus. The presence of acid in the lower esophagus causes disordered motor activity and increased clearance. Successful clearance protects the esophageal mucosa. Poor clearance, however, results ultimately in esophagitis. Skinner and Belsey (1988) suggest that the lower esophageal ring may therefore be the result of the repeated stimulus of acid refluxing into the lower esophagus that causes sustained disordered motor activity and a ring of spasm, but that because of the efficient clearance mechanism, no mucosal evidence of esophagitis is demonstrable. This phenomenon is similar to that which occurs at the cricopharyngeal zone, where reflux-related cricopharyngeal spasm occurs as a result of acid reflux across the lower esophageal sphincter.
Treatment of lower esophageal rings is based on the symptoms and the presumptive etiology of reflux. When pain is a presenting feature, or if the appearance of a radiologic ring is accompanied by evidence of reflux, active intervention to control reflux is indicated. The ring is dilated with bougies (Hurst or Maloney variety to 60F), and the gastroesophageal reflux is managed conservatively with a medical regimen. The protective effect of the ring on the esophageal mucosa above that level cannot be disregarded. If dilation results in bringing the reflux symptoms to the forefront despite conservative management of reflux, aggressive management is warranted, including, if necessary, surgery. Occasionally, the ring is not easily dilated, persists despite repeated attempts at dilation, and continues to be symptomatic. In these instances, at operation for repair of gastroesophageal reflux, a gastrotomy and digital or instrumental avulsion of the ring may be performed before the fundoplication. The need for such open excision is extremely rare in the absence of a stricture of the esophagus extending into the muscular layers as well as the mucosa.
TRAUMATIC STRICTURES
Trauma to the esophageal wall, if inadequately treated, may result in a benign esophageal stricture at the site of the original trauma. The likelihood of this occurrence is increased if mucosal approximation was not achieved early in the treatment of the trauma or if the episode was complicated by sepsis, resulting in considerable fibrous tissue reaction and subsequent contraction.
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Boerhaave's Syndrome
Spontaneous rupture of the esophagus can be repaired without any risk of subsequent stricture formation if care is sought promptly. If, however, presentation to the surgeon is delayed and the general condition of the patient has deteriorated, standard primary repair may not be the procedure of choice. Conservative management involving defunctioning esophagostomy, gastrostomy, and banding of the lower sphincteric zone with drainage of the mediastinum and pleural cavity usually results in considerable fibrosis around the site of rupture. If healing is achieved, the likelihood is great that narrowing of the lumen of the esophagus will occur. These strictures require elective intermittent dilation for a variable length of time.
Foreign Body Impaction
Even after the removal of a foreign body from the esophagus, the damage to the mucosal lining and the underlying tissues at the level of impaction can result in considerable inflammatory change and a localized area of intramural fibrosis and stricture formation.
Iatrogenic Strictures
The one disastrous complication that any endoscopist wishes to avoid is instrumental perforation of the esophagus. When recognized at the time of examination, it is remedied easily by open repair. If, however, the trauma goes unrecognized, the dangers of septic complication are high and subsequent stricture formation is unavoidable. Indwelling nasogastric tubes have been incriminated as a causative factor in stricture formation. In the patient with asymptomatic gastroesophageal reflux, the presence of an indwelling tube may cause intense esophagitis over a significant length of time. If, however, nasogastric intubation is used for only 24 to 48 hours after routine surgery, the chances of fibrous stricture formation are extremely low.
The surgeon may also be instrumental in causing stricture at the site of an anastomosis between the stomach and esophagus or between the esophagus and any other hollow viscus. The contributing role of suture material, ischemia, perianastomotic leak, microabscesses, and sepsis cannot be overemphasized. Use of prosthetic materials, such as tapes, around the freely mobilized esophagus and of antireflux prostheses is known to cause stricture formation. A further iatrogenic stricture is that associated with postmyotomy reflux after cardiomyotomy for achalasia. When the lower esophageal sphincteric mechanism is disrupted and no attempt is made to prevent reflux, esophagitis with the inevitable stricture formation occurs sooner or later.
Postirradiation Strictures
Postirradiation strictures result from cicatricial reaction to radiation therapy or to excessive dosage that destroys not only the lesion but also adjacent organs, such as the esophagus. These strictures tend to be long and irregular, with a tendency for the esophageal mucosa to develop adhesions and subsequent obliteration of the lumen. When recognized, radiation esophagitis has to be treated actively and early with elective dilation after the acute phase has subsided.
Management of Posttraumatic Strictures
Treatment of posttraumatic strictures can be summarized in chronologic fashion as follows:
Prevention
Conservation (elective dilation)
Resection and reconstruction or bypass
When damage to the esophagus is a likelihood, measures should be taken to avoid such events. Awareness of the possibilities goes halfway to avoiding trauma to the esophagus. If trauma has occurred, recognition and the adoption of measures to achieve optimal healing lead, in most instances, to a successful outcome. If, however, a stricture results from trauma, the treatment in most cases is successfully achieved with elective intermittent dilation. In those rare situations in which conservative measures fail, surgical intervention may be necessary. One may have to resect and reconstruct the upper gastrointestinal tract or, if the conditions in the mediastinum are such that resection is not feasible, a bypass using stomach, jejunum, or colon may be required.
CORROSIVE STRICTURES
Corrosive strictures of the esophagus occur equally in underdeveloped as well as affluent countries and result from suicidal or accidental ingestion of one of several agents. The most common corrosive agent implicated is caustic soda or lye. Bremner (1989) recorded that other substances are battery acid (sulfuric acid, hydrochloric acid, phosphoric acid), kitchen detergents, potassium permanganate, iodine, Lysol, paint strippers, potassium dichlorate, Clinitest tablets, and even dry ice. These agents cause considerable damage to the mouth, buccal cavity, pharynx, and the entire upper gastrointestinal tract down to the jejunum. They also affect the laryngotracheal inlet; if toxic fumes are inhaled, the lung parenchyma is also affected. The corrosive effect is produced by liquefaction, by alkalies, and by coagulation, by acids, of the lining tissues of the upper gastrointestinal tract, resulting in necrosis and
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sloughing of tissues and ultimately to ulceration of variable depth and even perforation into the mediastinum, pleura, or pericardium. Once ulceration has occurred, secondary infection occurs. Aided by reflux of gastric juice, an intense fibrotic reaction sets in, resulting in a stricture within 3 weeks to 3 months.Marchand (1955) described the classic features of acute corrosive burns of the esophagus, and Bremner (1989) classified them into three degrees. In the first degree, the burn affects the mucosa only. In the second degree, the damage extends into the tissues deep to the mucosa. In the third degree, necrosis extends into the periesophageal tissues, causing mediastinal, pleural, peritoneal, and adnexal perforation. This classification is based on information derived from clinical, radiologic, and endoscopic as well as operative findings. The acute assessment of the extent of injury, however, has several pitfalls. In the past, endoscopic examination was withheld until such time as obstructive symptoms developed. In more recent years, however, considerable experience has been accumulated by investigators such as Di Constanzo and Noirclerc (1980) in early endoscopic assessment.
Based on endoscopic evaluation, the burns have been graded as follows:
Stage I, catarrhal esophagitis confined to the mucosa
Stage II, ulceration, focal necrosis, and petechiae with changes extending up to the muscular layer
Stage III, extensive necrosis and bleeding, with black or brown mucosa over the entire circumference
Stage IV, complete carbonization of the mucosa
Lerut and colleagues (1989) suggest endoscopic evaluation be undertaken with a small-diameter flexible instrument within 12 hours, and certainly within 24 to 72 hours of the episode. This procedure is now standard practice. The emergency management of the patient entails the treatment of pain and circulatory shock, and maintenance of adequate metabolic and respiratory function. Secondary infection should be prevented. Preliminary investigations include radiography of the chest and abdomen to detect evidence of perforation or respiratory complications. To avoid the deleterious effects of extravasation, lavage and nasogastric intubation are avoided. Once stabilization of the general status is achieved, endoscopic evaluation is carried out and the degree of the injury is documented. Bremner (1989) suggests that contrast radiography be limited to water-soluble radiopaque agents that are easily eliminated in the event of extravasation.
The purpose of early flexible endoscopy is not only to assess the extent of corrosive burn, but also to determine the need for planned dilation. Because of the intensity with which fibrosis and stricture formation sets in, therapeutic dilation commences 3 weeks after the acute burn, at which time graded Maloney bougies are used to achieve optimal dilation without trauma. This process is repeated at intervals until a full dilation to 60F can be achieved. Dilation is not undertaken if preliminary investigations reveal extravasation outside the esophagus. In this situation, treatment of the extravasation precedes attempts at dilation.
Most patients who survive the acute period of circulatory shock benefit from a program of elective intermittent dilation. Some, however, require definitive surgical procedures, which entail resection of a variable length of the upper gastrointestinal tract from the pharynx down to the duodenum. When the stomach is unaffected and is available, it is the organ of choice for the replacement of the affected pharynx and esophagus. If, however, the stomach has been severely damaged, Bardini (1990), Gerzic (1990), and Lerut (1989) and their associates recommend a one-stage or two-stage replacement of the esophagus with a long-segment colon interposition from the neck to the abdomen, with either a retrosternal or posterior mediastinal placement of the colon.
INFLAMMATORY STRICTURES
Fibrous infiltration of the muscular layers of the esophagus can occur as a result of septic inflammation of the esophagus and after monilial infestation (Fig. 146-2). These conditions are common in debilitated and elderly individuals and in immunosuppressed patients. The strictures that result tend to be long but dilatable, and are managed with intermittent dilation because these patients do not present a favorable general condition to enable surgical intervention.
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In rare instances, however, resection and reconstruction may become necessary.Fig. 146-2. In patients with monilial esophagitis, a superficial, severe ulcerative appearance is present. This contrast-enhanced study demonstrates the fine serrated outline of the esophageal mucosa produced by the diffuse ulceration. |
A further cause of strictures resulting from localized inflammation is that which follows the impaction of tablets such as aspirin, as reported by Bonavina and colleagues (1987), and indomethacin. These agents cause acute erosion of the esophageal lining at the site of impaction, resulting in a localized stricture, in addition to which the drug causes an alteration in the ambient pH to an extremely acid state, resulting in extensive and serious damage.
Among the rarer causes of esophageal strictures are those associated with collagen diseases, such as scleroderma, dermatomyositis, systemic lupus erythematosus, Beh et's syndrome (Fig. 146-3), pemphigus vulgaris, and epidermolysis bullosa. These conditions ultimately lead to obstructive changes in the lumen of the esophagus. Depending on the manifestation in the acute phase, the changes may be predominantly in the mucosal and submucosal layers, such as in Beh et's syndrome and pemphigus and epidermolysis, or by fibrous infiltration of the muscular wall of the esophagus and lower esophageal sphincteric zone, as in scleroderma and dermatomyositis. In this latter group, the mechanism of stricture formation is by fibrous infiltration primarily by the disease and secondarily from reflux esophagitis. In the early stages of scleroderma, the esophagus remains an adynamic tube and empties entirely by gravity. When the disease affects the lower esophageal sphincteric zone, however, the sequelae of chronic gastroesophageal reflux result in shortening of the esophagus and narrowing of the gastroesophageal junction in exactly the same manner as in every other gastroesophageal reflux. The pathologic change, however, is progressive and affects the lower portion of the esophagus extensively, and the standard antireflux measures do not produce the required result. Recurrence of reflux invariably leads to further surgical intervention. The peptic stricture of scleroderma is dealt with in a manner similar to other peptic strictures (Fig. 146-4).
Fig. 146-3. In Beh et's disease, esophageal ulceration may be present in the absence of reflux. In this illustration, a 10-cm diffuse narrowing required repeated dilations to enable the patient to swallow. |
Fig. 146-4. A barium study shows the final result of an esophageal-lengthening V-Y gastroplasty and partial fundoplication in a patient with scleroderma affecting the esophagus and causing a peptic stricture. The air in the neofundus surrounds the lengthened neoesophagus below the diaphragm. |
PEPTIC STRICTURES OF THE ESOPHAGUS
The incidence of peptic strictures has undergone a revolutionary change since the late 1970s because of developments
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in the medical management of patients with gastroesophageal reflux. The latter change has occurred in part because of a better understanding of the mechanism of gastroesophageal reflux and in part because of breakthroughs in the control of acid production with H2 receptor blockers and proton pump inhibitors. Gastroesophageal reflux disease and its sequelae are not the manifestation of excess acid production, but the result of an abnormal presence of refluxed gastric contents in the lower esophagus. The role played by prokinetic drugs in clearing the refluxate from the lower esophagus of patients with gastroesophageal reflux is being increasingly recognized. Adequate control of gastroesophageal reflux disease with the combined use of acid-reducing and prokinetic drugs at an early stage of its genesis has undoubtedly resulted in less severe sequelae and less need for surgical resection of complex peptic strictures. Despite this change in the extent of gross sequelae, the average esophageal surgeon continues to see a constant trickle of patients with a variety of grades of peptic strictures that require surgical intervention in some form or other over and above the continued medical management of reflux.Perhaps the biggest factor in preventing the development of a complex peptic stricture is the ability of any clinician to determine when conservative medical treatment should stop and when surgery should be performed before irreversible changes occur in the esophageal wall. The changes not only destroy the lower esophagus but also disrupt the area of the lower esophageal sphincteric zone by fibrous tissue infiltration of the submucosa and the muscular layers, resulting in not only circumferential but also longitudinal contraction and, therefore, a shortened, strictured esophagus. The radiologist's concept of a peptic stricture is based on appearances at contrast radiographic screening, that held by a clinical endoscopist is based on what is seen at endoscopy, and that of the histopathologist is formed by the macroscopic and microscopic appearances of the resected specimen. An accurate correlation of all these different assessments is not easy. The esophageal surgeon, however, has to evaluate all these concepts and come to a decision, the results of which are likely to be influenced by the patient's aging process postsurgery.
Pathology
A true concept of the progressive changes that occur in chronic peptic esophagitis was developed by histopathologists in this field long before the histology of acute peptic esophagitis was clearly defined (Table 146-2). This discrepancy was caused in part by the availability of the resected specimens of complicated strictures, whereas tissue samples of acute esophagitis could be obtained only by endoscopic biopsies, which often produce inadequate tissues for proper evaluation.
Three forms of chronic peptic esophagitis were described by Sandry (1972): chronic superficial esophagitis, chronic localized penetrating ulceration, and combined chronic superficial esophagitis with ulceration.
Table 146-2. Components of a Pathologist's Concept of an Esophageal Stricture | ||||||
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Chronic Superficial Esophagitis
Chronic superficial esophagitis is characterized by destruction of the squamous mucosa, concentric collagen deposits in the submucosa progressing into the muscle layers, and fibrosis and lymphadenitis in the periesophageal tissues. These changes lead to progressive thickening of the esophageal wall and narrowing of the lumen. The changes occur not only circumferentially but also, with time, spread upward, resulting in lengthwise contraction (shortening) of the esophagus. Where a hiatal hernia may not have existed initially, herniation does occur with increasing shortening.
Chronic Localized Penetrating Ulceration
Chronic localized penetrating ulcerations may occur as follows:
Ulceration extends from the mucosa into the muscle layers that are by now infiltrated by inflammatory cells and fibrous tissue.
Ulceration occurs at the junction of the squamous and columnar mucosae and on the gastric side of the Z line.
Ulceration may be multiple and at several levels in the affected segment.
The associated fibrosis results in narrowing of the esophageal lumen.
Just as in peptic ulceration of the stomach, the minor vessels in the vicinity show endoarteritis obliterans, whereas any major vessels in the ulcer bed are capable of producing massive hemorrhage.
Combined Chronic Superficial Esophagitis and Penetrating Ulceration
Patients with combined chronic superficial esophagitis and penetrating ulceration show a combination of the features described in the preceding section. When mucosal healing occurs, it is achieved by columnar epithelium ascending from the squamocolumnar junction in linear streaks or as a tube (i.e., columnar tissue-lined esophagus). Dysplasia in such columnar epithelium-lined areas is not uncommon and predisposes the patient to malignant change (see Chapter 147). The exact relation between the rapid increase in the incidence of adenocarcinoma of the lower esophagus
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and the tendency toward persistence with nonsurgical management of gastroesophageal reflux disease is not clear.
Symptomatology
The characteristic symptoms of gastroesophageal reflux are obtainable with every patient with a peptic stricture. Some patients, however, deny any previous upper gastrointestinal symptoms, but a parent or other member of the same family often reveals that the patient did experience reflux symptoms in childhood. The so-called silent strictures are possibly related to a rather fulminant acute exacerbation of gastroesophageal reflux disease in a patient who was otherwise previously symptom free. The main components of these reflux symptoms are heartburn, indigestion, and pain in the retrosternal area and sometimes in the back between the shoulder blades. The intensity of the heartburn may to some extent have subsided recently, and pain becomes related to mealtimes when food is consumed. Pain is probably related to impaction and increased esophageal contractions rather than to esophagitis. Dysphagia tends to be progressive and of slow onset and is not necessarily associated with loss of body weight. It progresses from solids to soft foods and finally to liquids. Despite the difficulty in swallowing, protein deprivation is not common, but anemia may be significant because of mucosal ulceration and chronic loss of blood from esophagitis. Impaction of food depends on bolus size, length and girth of the stricture, and the motility of the esophagus above the stricture. In patients with impaired motility, such as in scleroderma or in the patient with combined corrosive and peptic strictures, the ease with which bolus obstruction occurs is related to this impairment of motility in the esophageal wall (Fig. 146-5).
Fig. 146-5. Where stricture is present, the descent of the food bolus is affected by lumen size, bolus size and consistency, and the motor power in the esophageal musculature. |
Because of the insidious onset of the obstructive symptoms, the patient often gives a history of inhalation and choking attacks for several months preceding any bolus obstruction or true dysphagia. These attacks may precipitate bronchospasm, and the patient may even be labeled asthmatic for some length of time before the diagnosis dawns on the clinician. A further mechanism for such asthma attacks may be related to reflex bronchospasm brought on by the presence of gastric contents in the lower esophagus, but a more probable cause of inhalation and choking is cricopharyngeal spasm, which is common in chronic gastroesophageal reflux disease. Some patients with peptic stricture of the esophagus present for the first time with symptoms and signs of bronchopneumonia resulting from such inhalations.
Investigations
The main purpose of investigations is to confirm the clinical diagnosis, nature, and probable etiology of the stricture. Investigations should also enable the clinician to decide on a possible mode of management of the stricture. The most important conclusion from the investigations, however, should be a categorical exclusion of an underlying malignancy.
Radiology
Once a proper clinical evaluation of the patient has been completed, the first investigation in the presence of dysphagia should be screening of the upper gastrointestinal tract with contrast radiography, except in those patients with sudden bolus obstruction of the gullet. A barium meal examination outlines the anatomy of the area and the precise features of the site of obstruction or narrowing before instrumental trauma is inflicted on the area (Table 146-3). A typical peptic stricture (Fig. 146-6) shows a smooth conical or tapering outline that may be interrupted by an
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ulcer crater on one or the other walls. Frequently, however, changes in outline are produced as a result of stasis ulceration, inflammation, submucosal gland hypertrophy, and filling defects attributable to food debris or food bolus above the stricture. Radiography also demonstrates any shortening of the esophagus or the presence of hiatal hernia, coexisting diverticula in the upper gastrointestinal tract, peptic ulceration in the stomach or duodenum, and evidence of pyloric dysfunction. Despite all these features, contrast radiography cannot indicate with certainty if the stricture is malignant or benign.Table 146-3. Components of Radiologic Stricture | |
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Fig. 146-6. This patient has a tight stricture at the squamocolumnar junction in association with a shortened esophagus and a fixed hiatal hernia. Radiologically, the lumen narrows smoothly and shows no evidence of deep ulceration, in contrast to the appearances in an esophageal carcinoma. |
Endoscopy
Visual inspection of the esophagus is essential for a full evaluation of the stricture. It is best achieved as part of full upper gastrointestinal endoscopy using the flexible instrument, aided if necessary with a second or even a third examination. This rule does not apply when bolus obstruction has supervened and emergency extraction of a foreign body above a stricture is necessitated. In these circumstances, rigid esophagoscopy and removal of the foreign body are quicker and relief of symptoms is more rapid. Every esophageal surgeon should be equally adept at upper gastrointestinal endoscopy using a flexible instrument and neuroleptic analgesia and at rigid esophagoscopy using general anesthesia. In addition to a visual inspection, the endoscopist should be able to feel the stricture and come to certain conclusions as to its features (Table 146-4). He or she should be capable of obtaining adequate samples of the strictured area for histologic, cytologic, and, if necessary, microbiological examination. At the same time, a preliminary dilation is performed to assess the nature of the stricture.
Table 146-4. Endoscopist's or Clinician's Concept of a Peptic Esophageal Stricture | |
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One can thus summarize the value of endoscopy as follows: estimation of the exact location, length, size, distensibility, and dilatability of the stricture; and estimation of the shortening of the esophagus, cytology of the brushings, histology of the biopsies, and features of gastroesophageal reflux. With these relevant facts, the endoscopist should be able to grade the stricture and the degree of esophagitis, exclude malignancy, and document the presence of any columnar epithelium-lined esophagus and the severity of dysplasia, if any.
Laboratory Investigations
In the presence of significant obstructive symptoms, ambulatory pH measurements and manometry (ambulatory or instantaneous) are unlikely to reveal any useful information. If, however, adequate dilation was achieved successfully at the time of initial endoscopy, then ambulatory pH establishes the state of reflux and to some extent the pH of the refluxate. The deployment of bile-detecting probes as part of pH measurement gives useful information regarding the role of this component in the causation of the stricture. Manometry reveals any underlying dysmotility of the esophageal wall proximal to the stricture, cricopharyngeal spasm, and other forms of disorders. These factors may prove to be useful in the management of the patient. Furthermore, once the stricture has been dilated, an initial course of rigorous medication and conservative measures to combat the gastroesophageal reflux may improve the extent of inflammation in the esophageal wall and alter its motility pattern for the better, ensuring a more representative result in assessing the esophageal function. All medication should be discontinued 1 week before the ambulatory pH and motility assessment.
Other investigations are directed toward evaluating the general condition of the patient, including cardiorespiratory
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function and function of the other systems, so that decisions regarding management of the stricture can be made appropriately.
Management
Initial management of peptic strictures is aimed at obtaining a histologic diagnosis and adequate passage to establish swallowing. Once these objectives have been achieved, every attempt should be made to heal the esophagitis to an optimal level with a full medical regimen, which should include general measures to improve the nutrition of the patient and to overcome the esophagitis and reflux with physical and postural measures, acid-reducing drugs, prokinetic drugs, and mucosal protecting agents. Every peptic stricture that has required endoscopic evaluation deserves reevaluation within 6 weeks, with repeat endoscopy to assess the response to treatment of the reflux disease and the response to dilation. This examination also enables the clinician to achieve optimal dilation without danger of instrumental trauma, especially if the preliminary endoscopic dilation was curtailed by the extent of the esophagitis.
Elective Intermittent Dilation
The further management of the patient with peptic stricture is dictated by the general condition of the patient. General debility associated with other chronic systemic disease, age, or cardiorespiratory status would dictate to the clinician the need to persevere with a program of elective intermittent dilation (Table 146-5). The main features of this program are continued conservative medical treatment and elective dilation of the stricture at increasing intervals, ensuring at all times that malignancy is excluded by repeat biopsies at the time of each dilation. Failure of this program is an indication for reassessment of the patient and the appropriateness of the program as opposed to surgical intervention (Figs. 146-7 and 146-8).
Table 146-5. Program of Elective Intermittent Dilations of Benign Peptic Stricture | |
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Fig. 146-7. Algorithm for decision making in the management of peptic stricture of the esophagus. |
Several types of bougies have been devised for esophageal dilation, ranging from the Maloney olivary-tipped, variation (Fig. 146-9) of the original Hurst bougies, to the gum elastic bougies for use through open rigid esophagoscopes,
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to the more recent Eder-Puestow system of olives loaded on a guidewire for radiographically controlled dilation using the flexible fiberoptic endoscope (Fig. 146-10). Other variations, such as those devised by Savary, have also gained popularity (Fig. 146-11).Fig. 146-8. Algorithm for decision making in the management of peptic stricture of the esophagus requiring surgery. |
Fig. 146-9. The upper bougie is a 60F Maloney bougie. It is compared with a 26F gum elastic bougie filling the lumen of an esophagoscope. The lower two bougies show a 26F Maloney and a 20F Hegar dilator. |
Surgical Therapy
The fact remains that the development of a stricture is a complication of gastroesophageal reflux disease and in itself warrants surgical correction of the reflux if the general condition of the patient permits it. In the absence of any contraindications, the patient should be made aware of lifelong medical treatment and its possible consequences, the hazards of repeated instrumentation, and the possible development of complications such as columnar lining dysplasia and malignancy in the lower esophagus. In my practice, the fit patient is offered surgery if no contraindication exists for use of a general anesthetic. The nature of the surgery, however, depends on the features of the stricture and the health of the esophagus above, in addition to coexisting problems in the gastrointestinal tract.
Fig. 146-10. Eder-Puestow olives ranging from 21F to 58F. The flexible introducer with the olive mounted is passed over a guidewire under radiographic control in increasing sizes until optimal dilatation is achieved. |
Fig. 146-11. Savary bougies are passed over a guidewire. The tapered Silastic tips allow safe dilation of the stricture. |
The aim of surgery is to overcome the gastroesophageal reflux and to conserve tissues in their normal anatomic locations wherever possible. If, however, the lower esophagus is irreversibly destroyed, then the objective would be to restore swallowing with the least chance of recurrence of the peptic stricture, if necessary by resection and reconstruction or by diversion of the digestive secretions of the upper gastrointestinal tract, thereby promoting rapid and maintained healing of the lower esophagus. It stands to reason that an esophagus that has been the seat of chronic esophagitis should continue to experience the long-term sequelae of fibroblastic infiltration, thereby undergoing further shortening and stenosing changes despite an antireflux surgical procedure. In reality, a small proportion of patients do show continued shortening and stricturing despite a successful antireflux procedure. Therefore, a certain degree of judgment is required when making a decision as to which antireflux procedure to choose and the need for an esophageal-lengthening procedure because of shortening and the intensity of esophagitis. The assessment of esophageal shortening has to be based on radiologic, endoscopic, and operative findings in the lower esophagus, and a final decision should be delayed until the time of the operative procedure. In my experience, however, a standard antireflux procedure alone in the presence of grade III or IV esophagitis is doomed to failure in the long term, but it may be a temporizing procedure, taking into account the domestic and other circumstances surrounding the patient at the time of surgery.
The antireflux procedure for patients with dilatable strictures should ideally be performed under adequate exposure that enables full mobilization of the lower esophagus. A transthoracic approach is the exposure of choice,
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but transabdominal repairs can be accomplished successfully, despite the stricture, if no undue shortening exists. The popular procedures are partial fundoplication, total fundoplication, posterior gastropexy, and fundic esophagoplasty. The fundic patch procedure in the presence of a short dilatable stricture was practiced for a few years, but it has been abandoned, superseded by one of the procedures just mentioned.
Partial Fundoplication: Mark IV Antireflux Procedure
Partial fundoplication, described by Skinner and Belsey (1967), is performed transthoracically, permits operative decision making and adequate mobilization up to the aortic arch, and ensures that no element of narrowing is produced by the fundoplication. It is contraindicated if gross shortening or extensive periesophageal fibrosis is present.
Total Fundoplication
Total fundoplication, reported by Rosetti and Hell (1977), may be performed using an abdominal approach or preferably, in the presence of a stricture, transthoracically. The latter approach allows for proper decision making regarding the need for an esophageal-lengthening procedure. This repair is contraindicated in the presence of shortening or periesophageal fibrosis.
Thal Fundic Patch
The Thal fundic patch, introduced by Thal and associates (1965), consists of a patch esophagoplasty over a vertical incision on the strictured esophagus by the construction of a patch of stomach applied to the esophagus, widening its lumen. This operation has been abandoned almost universally because of numerous complications and because the esophagitis and stricture continue unabated. Ximenes, however, reports its successful use in some patients with Chagas' megaesophagus (see Chapter 142).
Woodward's Modification of the Thal Patch
Woodward and associates' modification (1970) of the Thal patch was an attempt to overcome the continued reflux and ensuing esophagitis by performing an intrathoracic total fundoplication over the Thal-type esophagoplasty (Fig. 146-12). The total fundoplication is left in the chest. In principle and in Woodward's early experience, this maneuver appeared to be a solution, but subsequent experience by other surgeons has not added to the popularity of the procedure.
Posterior Gastropexy
Hill (1967) strongly advocated the posterior gastropexy, and the procedure has been favored by some as an entirely abdominal approach but one performed only in the absence of any shortening or periesophageal fibrosis. Perioperative monitoring, which is mandatory for this operation, is influenced by any degree of fibrous cicatrization present in the esophageal wall and is therefore unlikely to be of any practical help in performing this procedure in the presence of a stricture. In the presence of significant shortening of the esophagus, any form of standard antireflux procedure is achievable only under considerable tension on the esophagus. With time, the repair is bound to fail, and recurrence is the rule. Under these circumstances, some form of esophageal-lengthening procedure should be performed, followed by an antireflux maneuver.
Fig. 146-12. Woodward's modification of Thal's fundic patch incorporated a total fundoplication of the strictured area. The wrap remained in the chest, causing further problems at a later date, although it maintained adequate reflux control. |
Pearson's Modification of Collis' Gastroplasty
The vertical gastroplasty procedure was first put forward by Collis (1961) for other reasons and was subsequently adapted in combination with a partial fundoplication of the Mark IV type by Pearson (1977). In subsequent years, esophageal-lengthening gastroplasties have been used with partial as well as total fundoplication. For those patients in whom inherent motility and fibrous changes are present in the esophagus and are progressive in nature, such as in scleroderma, esophageal lengthening may be required even in the absence of significant shortening at the time of the primary repair, in an attempt to prevent recurrent reflux and subsequent reoperations. The introduction of Pearson's modification of Collis' gastroplasty, reported in 1971 and 1977, was a major advance in reducing the need for resection and reconstruction of the esophagus. The gastric neofundus is wrapped 240 degrees around the neoesophagus, and the fundoplicated segment remains under the diaphragm without any tension on the esophagus. Despite the difficulties in patients requiring
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this procedure, Pearson and colleagues (1987a,1987b) reported an 81% incidence of success without any residual dysphagia or reflux in 5 to 17 years of follow-up.Fig. 146-13. Total fundoplication reducing the wrap to 1.0 to 1.5 cm, as performed by Henderson. |
Henderson, alone (1986) and with Marryatt (1981, 1983), reviewed the long-term results of patients undergoing an esophageal-lengthening gastroplasty and partial fundoplication and came to the conclusion that reflux documented by instant pH studies in the long-term follow-up of these patients was too gross, and incorporated a total instead of a partial fundoplication after an esophageal-lengthening gastroplasty. In view of the obstructive symptoms noted in his patients, Henderson subsequently reduced the total fundoplication from a 3-cm to 1.0- to 1.5-cm wrap in the routine operation (Fig. 146-13). In patients with scleroderma and other motility disorders, the total fundoplication was further reduced to a one-stitch wrap. Orringer and Sloane (1978) similarly claimed better control of reflux with total fundoplication combined with a Collis-type esophageal-lengthening gastroplasty.
Fig. 146-14. Technique of V-Y gastroplasty and partial fundoplication devised and practiced by the author since 1981. The V-Y modification of an esophageal-lengthening vertical-cut gastroplasty produces a globular neofundus, ensuring a good inversion wrap of 240 degrees of partial fundoplication. |
In all these procedures of the Collis-type gastroplasty, the esophageal lengthening takes up the lesser curve of the stomach in the form of a tubular neoesophagus. The gastric fundus is rendered into a conical remnant of a neofundus that is more suitable for a total wrap of the Nissen type than for an inversion wrap of the Belsey Mark IV type of partial fundoplication. In 1984, Reilly and the author described a V-Y gastroplasty that created a tubular neoesophagus and a globular neofundus, which then rendered itself more amenable for a partial inversion-wrap procedure of the Mark IV partial fundoplication (Fig. 146-14). The early and long-term results of this procedure have been encouraging,
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and in one study, an antireflux rate of 94% and an 81% control of dysphagia were achieved in a follow-up of 1 to 10 years, which the author and associates reported in 1993.The esophageal-lengthening gastroplasties all incorporate some long-term disadvantages. These may consist of the following:
The lower esophageal sphincter and the dilatable stricture remain within or above the fundoplication and may cause a variable degree of dysphagia, which may require intermittent dilation.
The esophageal lining in the strictured segment may well have columnar elements to it, although preoperative biopsies would have excluded patients with severe dysplasia or carcinoma in situ from proceeding to this operation. Theoretically, however, such change could supervene at a later date. Diagnosis of early carcinoma after a gastroplasty and fundoplication must depend on meticulous endoscopic surveillance in all patients with columnar lining undergoing these operations (Fig. 146-15).
If a gastroplasty is undertaken without adequate preoperative preparation (i.e., endoscopic sampling on more than one occasion at several levels in a quadrantal fashion), the possibility of an underlying malignant stricture could be envisaged. The diagnosis of malignancy at postoperative follow-up will of necessity be delayed and be a source of litigation.
The possibility of an adenocarcinoma of the stomach developing in the neoesophagus, as reported by Groome and co-workers (1992), should always be entertained; with the present trend toward an increasing incidence of gastric carcinoma, this possibility is even more likely.
Fig. 146-15. Barium radiograph shows a columnar tissue-lined esophagus. In this acquired condition, the lining epithelium is replaced by a columnar variety after long-standing reflux esophagitis. Underlying fibrosis leads to shortening and stricture formation. The squamocolumnar junction is elevated to a variable extent into the chest. |
Acid Suppression and Biliary Diversion
Acid suppression and biliary diversion has been recommended as a less invasive surgical procedure capable of diverting the digestive secretions reaching the lower esophagus even when gastroesophageal reflux is present. Wells and Johnston (1955) first reported the clinical results of vagotomy, gastrectomy, and Roux-en-Y gastrojejunostomy without resection of a dilatable stricture. Several subsequent reports, mainly emanating from the Mayo Clinic by Payne (1970, 1984), cited excellent results in small numbers of patients. Washer and associates (1986), with the largest number of patients, reported biliary diversion in patients who not only had strictures but also had recurrent severe esophagitis. Ellis and Gibb (1990) described 23 patients with severe recurrent esophagitis who underwent antrectomy and Roux-en-Y gastrojejunostomy, 18 of whom also required resection of the lower esophageal sphincteric zone for stricture, without any hospital mortality. They reported an 86% improved symptomatology. The 57% excellent to good result, however, compares unfavorably with either the aforementioned conservative procedures or the resectional procedures practiced when indicated, as noted in the next section.
Resection
Indications for resection are enumerated in Table 146-6. In addition to the five mentioned in the table, in those patients in whom two or more procedures to overcome recurrent reflux disease have been unsuccessful, serious consideration should be given to resection and reconstruction, not only to overcome reflux but also to avoid conserving an ischemic, dysmotile lower esophagus rendered thus by repeated surgical mobilization that resulted in vascular deprivation and denervation.
The objectives of resection and reconstruction are twofold: (a) total and sustained relief of dysphagia, and (b) prevention of reflux of gastric contents into the residual esophagus. In achieving these objectives, the procedures should carry an acceptable mortality and morbidity, avoid
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creating new problems, be applicable to infants and adults, and avoid multiple interventions.Table 146-6. Indications for Resection | |
|---|---|
|
The extent of esophagus resected depends on the length affected by the cicatrization. In some instances, although the fibrosis extends a short way, stasis ulceration and metaplastic changes in the lining epithelium of the esophagus would justify more extensive resection proximally. Similarly, ischemic changes caused by multiple previous operations on the gastric fundus would dictate resection of that part of the gastric fundus to avoid ischemic complications in this area.
The organ for replacement of the resected esophagus should ideally be dispensable and transposable without undue difficulty, preferably retaining its normal blood supply on a pedicle without the need for vascular reconstruction. The stomach, being an organ situated in the upper abdomen, has been used for reconstruction after resection of peptic strictures for several decades. It has a good blood supply and can be mobilized to reach any level from the lower part of the chest to the pharynx. Reconstruction using the stomach requires only one anastomosis, be it in the chest or in the neck. It does, however, have the disadvantage that gastric contents are capable of being regurgitated into the esophageal remnant across the anastomosis. The higher the level of anastomosis, the lower the degree of reflux, but reflux esophagitis in the residual esophagus may be unavoidable unless the anastomosis is performed in the neck, where ischemic anastomotic fistulae and strictures tend to occur. The displacement of the stomach to this new location achieves anatomic continuity at the expense of causing several physiologic disturbances.
The jejunum has been used as an isoperistaltic segment interposed between the esophagus and the stomach, and because of its rich blood supply, it can be mobilized on a pedicle for considerable distances. When a sufficient length of jejunum has been retained below the diaphragm, it acts as an antireflux viscus, preventing gastric juices from reaching the esophageal remnant. It does, however, have the disadvantage of having a propensity to produce anastomotic peptic ulcers. Furthermore, in obese adults, the fat-laden mesentery renders mobilization of the vascular pedicle extremely tedious. In infants, however, the jejunum is an excellent substitute.
The colon has a good blood supply in the young adult before arteriosclerosis sets in and, based on a blood supply derived from one of three major vessels (the right colic, the middle colic, or the left colic arteries), offers an excellent substitute organ in variable lengths derived from the right hemicolon, transverse colon, or left hemicolon, respectively. When a short segment is required for bridging a subaortic gap in the esophagus, the right or left hemicolon is all that is required, enabling a full 14-cm length of distal colon to be retained below the diaphragm and reaching the stomach low on the posterior surface for its distal anastomosis, thereby acting as an efficient antireflux segment (Fig. 146-16). When the upper anastomosis has to reach the apex of the chest or neck, the right or left hemicolon and part of the transverse colon based on a single vascular pedicle can be adequately mobilized with a blood supply reaching the neck on a marginal arcade (Fig. 146-17). Thomas and colleagues (1997) concluded that colon interposition for esophageal substitution provides satisfactory function when the stomach is not available. In a follow-up study of patients subjected to colon interposition over a 30-year period, the author and associates (1998) have shown that although a short segment acts as a good functional and anatomic entity, long-segment substitutes develop anatomic and functional complications.
Fig. 146-16. Contrast radiograph of a patient who had the lower esophagus replaced with a short segment of left hemicolon for undilatable peptic stricture. The colon functions as a straight conduit without any tendency to redundancy. |
Fig. 146-17. Contrast-enhanced radiograph reveals the state of the upper gastroesophageal tract in a patient who had the entire esophagus replaced in childhood with a long segment of left hemicolon for extensive corrosive stricturing. Notice the tendency for the colon to develop redundancy in the chest in adult life 23 years later. |
Apart from these three substitutes, a reversed gastric tube introduced by Gavriliu and Georgescu in 1951 and further
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discussed by Gavriliu (1965) is also a suitable substitute, but more so in corrosive than in peptic strictures. It does have the advantage that the stomach can be retained in the abdomen, but it has the disadvantage of a long suture or staple line with a higher possibility of leakage.In my practice, the choice of organ is dictated by availability and adequacy. In the fit young patient with a good blood supply, I prefer to select the left hemicolon based on the upper left colic arterial pedicle, ensuring that preliminary trial clamping of the middle colic does not cause ischemia. In the older patient, when the colonic blood supply has been suspect and when diverticular disease is fairly common in the left colon, the stomach has been the organ of choice. When the stomach has been subjected to previous surgery, however, such as partial gastrectomy or gastrojejunostomy, or on those occasions when gross adhesions from previous upper abdominal surgery have prevented adequate mobilization, an alternative organ has been sought.
The physiologic changes after reconstruction of the esophagus have been studied carefully, in terms of both the functional efficiency of the substitute and the nutritional disturbances caused by transposing a part of the digestive tract. Laboratory and clinical studies in my department reported by Peppas and colleagues (1993) have shown that interposed colonic segments demonstrate a motility pattern similar to that of the colon in its normal location, with minor modifications. The Visick score of patients, with a follow-up of 1 to 14 years after such surgery, is 84.5% in grades I and II, whereas good reflux control, as studied by ambulatory pH, was achieved in 92%. These results compare with reflux control of only 50% in those patients in whom the stomach was brought up into the chest for an end-to-side anastomosis with a partial wrap.
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