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Surgical Pathology of Esophagus: 4 Hours
Surgical Pathology of Esophagus: 4 Hours
4 hours
C 1 2 hours Esophageal trauma: corrosive esophagitis: etiology, clinical aspects, evaluation, diagnosis, treatment. Motility disorders: diffuse esophageal spasm, achalasia of cardia(definition,etiology, clinical aspects, evaluation, diagnosis, differential-diagnosis,complications, treatment) Esophageal diverticula: definition, etiology, clinical aspects, evaluation, diagnosis, differential diagnosis, complications, treatment C 2 2 hours Tumors of esophagus: Benign tumors of the esophagus: pathology, evaluation diagnosis treatment. Malignant tumors of the esophagus: classification, clinical aspects, pathology, evaluation, diagnosis, differential diagnosis, treatment.
Pathophysiology Regardless of the specific cause, the resulting mediastinitis and his severe consequences demand prompt recognition and treatment of the esophageal disruption. Esophageal and gastric contents are sucked into the mediastinum by respiratory movements and negative intrathoracic pressure. Salivary enzymes, gastric acid, bile, and food enter the mediastinum, the presence of oral bacteria in these fluids initiates a fulminant infection and an inflammatory response progresses. This mediastinal burn produces massive fluid accumulation, which can displace the trachea, heart, or lungs The entire process is aggravated if there is preexisting esophageal disease causing obstruction distal to the perforation. Clinical Features Patients with esophageal perforation characteristically present with: cervical or thoracic pain, difficulty swallowing, respiratory distress, fever. Pain features depends with esophageal perforation location Cervical or upper thoracic esophagus generally cause cervical or high retrosternal pain Middle or distal esophagus produce anterior thoracic, posterior thoracic, interscapular, or epigastric pain. Upper thoracic esophageal perforations may produce signs of right pleural effusion, while Distal esophageal perforation is associated with left pleural effusion.
Diagnosis
Pain or fever after esophageal instrumentation or operation is indicative of an esophageal perforation and is an indication for an immediate contrast esophagogram with hidro - soluble contrast substance. A chest roentgenogram may help to confirm the diagnosis by demonstrating air in the soft tissues of the neck or mediastinum(pneumomediastinum) or a hydrothorax or pneumothorax. A contrast-enhanced CT scan may lead to the diagnosis The morbidity and mortality rates associated with esophageal perforation are directly related to the time interval between diagnosis of the injury and its repair or drainage
Barium esophagogram demonstrates a perforation (arrow) in the middle third of the thoracic esophagus.
Management(Principles of Surgical Treatment) The initial treatment of an acute esophageal perforation focuses on: decreasing bacterial and chemical contamination of the mediastinum restoring intravascular volume losses.
Oral intake is withheld, the patient is instructed not to swallow saliva. A disposable oral dental suction is often helpful for evacuating oral secretions. Broad-spectrum intravenous antibiotics with activity against oral flora are administered using a combination of a cephalosporin (cefazolin or cefamandole), 1 g/4 h, and an aminoglycoside (gentamicin or tobramycin), 1 to 1.5 mg/kg/8 h, and metronidasole 2g/24h. Nasogastric tube decompression of the stomach is instituted to minimize possible gastroesophageal reflux and further soiling of the mediastinum. Therapy of esophageal perforation is influenced by: The location of the tear The size of the tear The cause of the tear, The length of delay in diagnosis, The extent of mediastinal and pleural contamination The presence of intrinsic esophageal disease. The treatment of an acute esophageal perforation must be individualized.
Nonoperative Therapy Although most esophageal perforations require operative intervention; only selected patients may be managed nonoperatively with: Cessation of oral intake, Administration of antibiotics, Intravenous hydration until the disruption heals or the small contained cavity begins to decrease in size. Criteria for nonoperative therapy of an esophageal perforation include the following: A local, contained disruption without evidence of pleural contamination (hydrothorax or pneumothorax), A walled-off extravasation in which contrast material drains back into the esophagus, Minimal or no symptoms, Minimal or no evidence of systemic infection (fever or leukocytosis). The usual clinical settings in which such perforations are encountered are: cervical esophageal tears caused by esophagoscopy; intramural dissections that have occurred during dilation of a stricture or pneumatic dilation for achalasia; asymptomatic esophageal anastomotic disruption discovered on a routine postoperative contrast study.
When treating such perforations conservatively, oral hygiene should be optimized to minimize further contamination by oral bacteria A nasogastric tube is seldom helpful. Nutrition may be maintained by a nasogastric feeding tube, gastrostomy, or jejunostomy or by intravenous hyperalimentation until oral intake can be resumed, usually 1 to 3 weeks after the injury. nonoperative therapy is best suited for patients presenting no more than 24 hours after the injury with no systemic evidence of sepsis and clearly demonstrable, contained, internally drained leaks on barium esophagogram. Infants with iatrogenic perforation can often be successfully managed without operation. Perforations complicating pneumatic dilation for achalasia occur in 4% to 6% of patients, and most are small and well-managed medically with antibiotics and intravenous hyperalimentation. For the remainder of patients with perforations, operative therapy is generally indicated. OPERATIVE THERAPY OF ESOPHAGEAL PERFORATIONS Cervical and Upper Thoracic Esophageal Perforations lead to: Progressive contamination of the mediastinum as infection descends dependently along the fascial planes from the neck. Unless adequate drainage is accomplished, death from mediastinitis follows. Most cervical and upper thoracic perforations may be adequately drained through a cervical approach, placing drains in the retroesophageal space.
An incision is made parallel to the anterior border of the sternocleidomastoid muscle, which is retracted laterally along with the carotid sheath and its contents. The trachea, thyroid gland, and strap muscles are retracted medially. It may be necessary to divide the omohyoid muscle, middle thyroid vein, and occasionally the inferior thyroid artery to reach the prevertebral fascia. Once this is identified, blunt finger dissection into the prevertebral space gives access to the abscess cavity, and appropriate drains are placed and brought out through the skin incision. When a cervical esophageal perforation extends into either pleural cavity or the lower mediastinum, the cervical approach is inadequate, and transthoracic drainage is required.
Operative Therapy Of Esophageal Perforations(suite) Thoracoesophageal Perforations Normal esophagus The earlier an esophageal perforation is recognized and treated, the better is the chance for successful primary repair. Most agree that such perforations that are not associated with intrinsic esophageal disease are best treated with primary repair of the tear combined with wide mediastinal drainage. A change in philosophy has occurred regarding the application of primary repair to perforations occurring in an normal esophagus regardless of the duration of the injury. Perforations of the lower third of the esophagus are approached through a left thoracotomy in the sixth or seventh interspace, while more proximal thoracic esophageal tears are approached through a right thoracotomy. Mediastinal drainage is achieved by opening the mediastinal pleura from the level of the tear to the thoracic inlet superiorly and the diaphragm inferiorly, irrigating the mediastinum, and placing a large-bore chest tube that allows transpleural drainage. Perforations of the intraabdominal esophagus unassociated with pleural contamination are approached through the abdomen. Esophagus With Intrinsic Disease Perforations associated with distal obstruction from intrinsic esophageal disease constitute a problem because breakdown of an attempted repair is common in the presence of distal obstruction. The associated obstruction must be relieved at the same time of repair and drainage.
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Operative Therapy Of Esophageal Perforations(suite) Patients with intrinsic esophageal disease that cannot be treated effectively by more conservative means are best treated by esophageal resection. Immediate esophageal substitution with colon(retrosternal) or stomach (in the posterior mediastinum) in the native esophageal bed.
Final position of the mobilized stomach in the posterior mediastinum after transhiatal esophagectomy and cervical esophagogastric anastomosis. 11
Operative Therapy Of Esophageal Perforations(suite) In situations in which immediate esophageal reconstruction is not possible, the stomach is divided from the esophagus, the cardia is oversewn, The intrathoracic esophagus is then mobilized through the diaphragmatic hiatus and a cervical incision, delivering the entire thoracic esophagus through the neck wound and placing it on the anterior chest wall. The mediastinum can be copiously irrigated through the cervical incision and the diaphragmatic hiatus at the time of esophagectomy A feeding jejunostomy is used for enteral alimentation until reconstruction is performed several weeks later.
Irrigation of the posterior mediastinum after transhiatal esophagectomy for irreparable esophageal disruption.
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Late Esophageal Perforation The longer the time interval between the occurrence of the perforation and operative treatment, the more inflamed are the tissues adjacent to the tear and, at least theoretically, the greater is the risk of failure of primary suture repair. Patients with late-recognized esophageal perforations have been treated in a variety of ways, with wide drainage alone, drainage and closure, drainage over a T-tube, esophageal resection, exclusion and diversion, and even nonoperative management.
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Detail of stomach showing the typical hourglass deformity due to severe antral stenosis
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Clinical Features The clinical manifestations of caustic ingestion are directly related to the amount and character of the agent ingested. Solid alkali typically causes burns of the mouth, pharynx, and upper esophagus. The resulting severe pain usually causes immediate expectoration so that relatively little of the caustic agent is swallowed. On examination, the mucosa of the mouth and oropharynx shows patchy areas of white to gray-black pseudomembranes. Patients may present with Excessive salivation Hoarseness, Stridor, Aphonia, and Dyspnea from laryngotracheal edema or destruction. Liquid alkali ingestion. This form of alkali is usually swallowed quickly, producing less injury to the mouth and pharynx but more damage to the esophagus, stomach, or both. Patients may present with Dysphagia, Odynophagia, and Aspiration, Severe retrosternal, back, or abdominal pain and signs of peritoneal irritation suggest that mediastinitis or peritonitis resulting from esophageal or gastric perforation has occurred.
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Acid ingestion, gastric injury is more common; therefore, signs and symptoms are frequently localized to the abdomen. When esophageal or gastric perforation results from caustic ingestion, progressively severe sepsis and hypovolemic shock until appropriate resuscitative measures are instituted. In the absence of gastric or esophageal perforation, the acute clinical manifestations typically resolve within several days, with clinical improvement lasting for several weeks. After this, symptoms due either to esophageal or gastric stricture formation begin. Although only 10% to 25% of adult patients who ingest solid alkali develop strictures, most patients who ingest liquid alkali have severe esophageal and usually gastric injury that often results in stricture formation. Children with limited exposure from accidental ingestions are less likely to have severe injuries. Acid ingestion most often results in stricture or contracture of the antrum or pylorus. Immediate Diagnosis And Treatment Acute caustic ingestion is an indication for hospitalization. Initial management centers on stabilizing the patient and assessing the severity of the injury. Vomiting should not be induced. Because caustic injuries produce almost instantaneous tissue damage, Attempts to dilute the agent by having the patient drink water are futile and dangerous. In fact, this may only aggravate the problem by producing increased gastric distention and vomiting. Oral intake should be withheld and hypovolemia corrected with intravenous fluids.
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Immediate Diagnosis And Treatment (suite) Careful observation for evidence of airway obstruction is mandatory. Endotracheal intubation or tracheostomy may be required if there is significant laryngeal edema or actual laryngeal destruction. Broad-spectrum antibiotics are indicated once the diagnosis of substantial esophageal injury has been established to diminish the risk of pulmonary infection from aspiration as well as bacterial invasion through the damaged esophageal wall. Although corticosteroids have been advocated in the acute phase of caustic ingestion to minimize subsequent stricture formation, their efficacy has not been established. Because corticosteroids may mask signs of sepsis and visceral perforation and impair healing, their use in caustic esophageal injury is potentially deleterious and is therefore not recommended. A relatively urgent contrast examination of the esophagus may provide important information in the patient with a caustic injury. Radiographically, acute mucosal esophageal injuries are seen as blurred irregular margins with linear streaking of contrast in deeper ulcers. Submucosal edema may be manifest by scalloped or straightened esophagogastric junction margins. Dilation of the esophagus and stomach, gastric ulcerations, air in the gastric wall, and frank extravasation of contrast material from the esophagus or stomach are common. A contrast esophagogram is the best way to make the diagnosis of esophageal perforation and should be performed if the diagnosis is suspected either at the time of admission or in subsequent follow-up. Identification of the site of perforation is vitally important in the planning of subsequent intervention. The initial esophagogram in these patients can be performed with a water-soluble agent (eg, Gastrografin), but dilute barium provides much better mucosal detail and should be used if the diagnosis of perforation is suspected.
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Management Esophagogastroscopy should be performed soon after admission to establish whether significant esophageal injury has occurred and to permit grading of the severity of the injury
Third-degree
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Management (suite) After the initial resuscitative and diagnostic measures are performed, patients with caustic injuries must be observed carefully. Those with first-degree burns require no other specific therapy for 24 to 48 hours. The incidence of subsequent esophageal stricture is low in patients with such injuries. Those who have second- or third-degree burns require careful and more prolonged observation for evidence of esophageal or gastric necrosis during the acute phase of the injury. Full-thickness necrosis of the esophagus, stomach, or other organs requires emergent resection. Patients with free intraperitoneal air, mediastinal air, extravasation of contrast material from the stomach or esophagus, peritonitis, or abdominal or mediastinal sepsis require immediate surgical exploration. Similarly, exploration is indicated in patients with severe persistent back or retrosternal pain suggesting mediastinitis and in those with metabolic acidosis suggesting visceral necrosis. When esophageal or gastric resection for acute caustic injury is required, restoration of alimentary continuity should be deferred until the patient has recovered from the acute insult and the development of chronic stricture formation in retained organs can be evaluated. Esophageal stricture formation after second- and third-degree burns is the rule, and dilation therapy has been the traditional therapy for chronic caustic esophageal strictures. Dilation therapy should not be instituted until at least 6 to 8 weeks after the injury, when reepithelialization is complete, to minimize the risk of esophageal perforation If a caustic esophageal stricture is perforated during dilation, esophagectomy and visceral esophageal substitution is the best approach because repair of a perforation proximal to a stricture is rarely successful.
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Management (suite) Strictures that cannot be adequately dilated (to a 46F dilator or larger for adults) and those that remain refractory to dilation after 6 to 12 months require esophageal substitution, usually with colon or stomach which is the preferred esophageal substitute, but its use in these patients may be precluded by gastric scarring and contracture secondary to the original injury. Severe esophageal strictures resulting from caustic ingestion have been managed in the past by retrosternal colonic interposition, leaving the native, destroyed esophagus in situ in the posterior mediastinum. Recent data, favor resection of the damaged esophagus in virtually every case, for several reasons: First, the obstructed esophagus can develop into a posterior mediastinal retention cyst or abscess. Second, caustic injuries may result in destruction of the lower esophageal sphincter, resulting reflux esophagitis in the retained esophagus Finally, the risk of esophageal carcinoma developing after a caustic injury is about 1000 times the usual risk, with an incidence of 0.8% to 4%, typically after a latent period of 20 to 40 years. Therefore, a young patient whose caustic esophageal stricture is simply bypassed must be followed indefinitely for the development of carcinoma in the native esophagus, Resection of the strictured esophagus also permits placement of the esophageal substitute in the posterior mediastinum in the original bed. This is the shortest and most direct route between the neck and abdominal cavity and does not require resection of the clavicle and adjacent sternum to enlarge the superior opening into the anterior mediastinum, as is required when carrying out a retrosternal esophageal substitution.
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An esophageal diverticulum is an epithelial-lined mucosal pouch that protrudes from the esophageal lumen. Most esophageal diverticula are acquired, and they occur predominantly in adults. Esophageal diverticula may be classified according to their location: Pharyngoesophageal (Zenker) diverticula occur at the junction of the pharynx and esophagus; Parabronchial (mid-esophageal) diverticula occur in proximity to the tracheal bifurcation; and Epiphrenic (supradiaphragmatic) diverticula occur in the distal 10 cm of the esophagus. Diverticula containing all layers of the normal esophageal wall (mucosa, submucosa, and muscle) are termed true diverticula, while those consisting of only mucosa and submucosa are false diverticula. Most esophageal diverticula arise because elevated intraluminal pressure forces the mucosa and submucosa to herniate through the esophageal musculature; these are false diverticula. Traction diverticula result from external inflammatory reaction in adjacent mediastinal lymph nodes that adhere to the esophagus and pull the wall toward them as healing and contraction occurs, and these are true diverticula. Pharyngoesophageal and epiphrenic diverticula are pulsion diverticula that are generally associated with abnormal esophageal motility. Parabronchial diverticula are usually but not always of the traction variety and include all layers of the esophageal wall.
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Formation of pharyngoesophageal (Zenker) diverticulum. (A) Herniation of the pharyngeal mucosa and submucosa occurs at the point of potential weakness (Killian triangle; arrow) between the oblique fibers of the thyropharyngeus muscle and the more horizontal fibers of the cricopharyngeus muscle
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Small Zenker diverticulum. (A) The 2.5-cm pouch and the esophageal narrowing distal to it representing the tight cricopharyngeus sphincter. (B) Detail of pouch showing retained barium.
Posteroanterior (A) and oblique (B) views from barium esophagogram in an 15-cm pharyngoesophageal diverticulum 26
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Barium esophagogram showing an epiphrenic diverticulum as well as a small traction diverticulum (arrow) of the middle esophagus.
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Completed cricomyotomy
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Barium esophagogram demonstrating a dilated esophagus and the characteristic birds beak deformity in a patient with achalasia.
Barium esophagogram in a patient with advanced achalasia showing a dilated sigmoid esophagus and an epiphrenic diverticulum (arrow).
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Myotomy of the LES, extending from below the aortic arch proximally and 1 to 2 cm beyond the gastroesophageal junction on to the stomach.
Laparoscopic approach
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Barium esophagograms of two patients with diffuse esophageal spasm, showing corkscrew esophagi with multiple contractions
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Gastroesophageal reflux is a normal phenomenon. This can be measured only by 24-hour pH monitoring. Most normal people experience short episodes of reflux, usually after meals. Gastroesophageal reflux disease occurs when esophageal acid exposure exceeds that of a normal population.
Other definitions used in the past were either nonspecific (eg, symptoms of heartburn or regurgitation) or indirect (eg, the presence of a hiatal hernia), or they detected the disease only when complications such as esophagitis were present.
The ready availability of 24-hour esophageal pH monitoring allows the physician to quantitate the abnormality, to assess objectively the response to treatment, and to formulate a logical approach to therapy. It is estimated that 7% of Americans suffer from daily heartburn, and up to 30% use antacids at least once a month. Most people whose symptoms are controlled by such means do not consult a physician, and of those who do, few are referred to surgeons. Pathophisiology Pathologic gastroesophageal reflux may result from the following causes: a mechanical defect in the LES. This accounts for about 50% to 60% of patients with increased esophageal acid exposure. It is important to identify these patients because they generally have a good outcome after antireflux surgery but a poor response to medical treatment. inefficient esophageal clearance of refluxed gastric juice and abnormalities of the gastric reservoir that augment physiologic reflux. Clinical features Symptoms of GERD can be classified as either: Typical (ie, heartburn and regurgitation) or Atypical (ie, noncardiac chest pain, pulmonary problems such as asthma, recurrent pneumonia or progressive fibrosis, laryngeal symptoms such as hoarseness and aspiration, and loss of dental enamel).
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Angina-like chest pain, sometimes called noncardiac chest pain, is frequently caused by GERD. These patients often describe other classic symptoms of GERD, which tend to be mild and overshadowed by the chest pain. Of patients with angiographically negative chest pain, 20% to 50% have an esophageal cause, and of these, 50% have increased esophageal acid exposure. Epigastric pain and nausea may be associated with other symptoms of GERD and usually result from pathologic DGR or delayed gastric emptying. It is important to recognize these symptoms before offering a patient antireflux surgery because they may persist after operation, and the patient should be warned of their presence and the possibility of future medical or surgical therapy.
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COMPLICATIONS OF GASTROESOPHAGEAL REFLUX DISEASE IN 150 CONSECUTIVE ADULT PATIENTS Patients 59 47 19 25 Normal LES (%) 58 23* 11 0 Defective LES (%) 42 77 89 100
LES, lower esophageal sphincter. * Grade of esophagitis more severe with defective LES.
LES failure is an early event in the pathogenesis of GERD and that patients with tissue injury have more profound impairment of LES function.
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Repetitive injury from noxious gastric juice can lead to mutations during the repair process in the p53 gene, a gene that controls programmed cell death. Patients with adenocarcinoma arising in Barretts esophagus have a high incidence of p53 mutations. Short Esophagus The term short esophagus is used by surgeons to describe the situation in the operating room when the gastroesophageal junction cannot be brought down into the abdominal cavity without tension. Esophageal shortening begins to occur early in the development of GERD Manometric studies demonstrate that shortening of the esophageal body increases as complications become more severe. Shortening of the longitudinal muscle, is associated with hiatal herniation, and periesophageal inflammation. Radiologically, it is associated with fixation of the hiatal hernia; that is, the hernia does not reduce in the upright position after a swallow. Any hernia greater than 5 cm in length is likely to be associated with esophageal shortening.
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Manometric length of the esophagus in patients with gastroesophageal reflux disease compared with normal subjects. Esophageal length progressively shortens as the complications of the disease become more severe. *P < .001 versus normal subjects.
Manometrically, the peristaltic amplitude in the distal esophagus is often subnormal. If this condition is detected only at the time of an abdominal fundoplication, the surgeons options are severely limited. It is much better to detect it ahead of time and plan the operative strategy accordingly
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Only two randomized trials have compared the relative merits of medical versus surgical treatment. Both showed a clear advantage for surgical treatment, but some are reluctant to accept this conclusion, arguing that the medical treatment in both did not include omeprazole. An ongoing trial comparing laparoscopic Nissen fundoplication with proton pump inhibitors may provide a conclusion more relevant to current practice. There is no doubt that proton pump inhibitors represent a great advance in the medical treatment of GERD, but until recently, long-term use was discouraged by the US Food and Drug Administration.
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Operative Indications The first requirement in the consideration of antireflux surgery are: Objective demonstration of the presence of GERD by 24-hour pH monitoring. Second, The patient must have either symptoms or complications of the disease. The disease should be caused by a defect remediable by surgical therapy, such as a mechanically defective LES. Studies have indicated that a Nissen fundoplication has beneficial effects in addition to restoring the characteristics of the LES. It may accelerate gastric emptying and reduce the frequency of transient LES relaxations. Consequently,
even in patients without defective sphincters, there are situations in which a Nissen fundoplication can correct the underlying abnormality.
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Algorithm for selecting patients with symptoms suggestive of gastroesophageal reflux disease (GERD) for further study. 58
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Nissen Fundoplication
A. B.
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Once the esophagus is encircled and the tumor located, the overlying longitudinal muscle is split in the direction of its fibers. The tumor is then gently dissected away from the contiguous underlying submucosa and adjacent muscle. When enucleation of the tumor is complete, the longitudinal esophageal muscle is reapproximated, although a large extramucosal defect may be left without complication. When resection is complete, leiomyomas virtually never recur. Polyps Benign polyps of the esophagus are rare and typically arise in the cervical esophagus. Traction on these polyps caused by repeated peristaltic contractions results in progressive lengthening of their pedicles. This may be responsible for their dramatic presentations, extruding into and even out of the mouth or producing asphyxia as the upper airway becomes obstructed. Most benign polyps occur in older men, and these frequently are attached to the cricoid cartilage. The tumors typically produce dysphagia, but hematemesis or melena may occur if the overlying mucosa becomes ulcerated. These polyps tend to be solitary with a long, cylindric configuration that may produce marked esophageal dilation. Histologically, they are composed of fibrovascular tissue with varying amounts of associated fat. Barium swallow findings may be nondiagnostic or inaccurately interpreted in these patients. The polyp may be overlooked as an air bubble or may be misdiagnosed as a carcinoma, or even as a foreign body or achalasia if it has caused marked esophageal dilation . Similarly, esophagoscopy may fail to define the polyp, particularly if the pedicle is not demonstrated and the mucosa overlying the polyp is normal. The endoscopist simply passes the lesion, which is soft and easily displaced with the esophagus. Although esophageal polyps have been removed endoscopically by electrocoagulation of the pedicle, the recommended approach is resection through a lateral cervical esophagotomy, delivering the polyp from the esophagus, resecting its mucosal base of origin, and repairing the defect under direct vision
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Barium esophagogram of a patient with a giant benign fibroepithelial polyp, showing a large intraluminal mass distending the cervical and upper thoracic esophagus.
The giant polyp has been delivered out of the cervical esophagus through a left-sided neck incision. The patients head is toward the right, and the retractors are
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Hemangiomas Esophageal hemangiomas are rare, constituting 2% to 3% of benign tumors. They are generally asymptomatic, they can be responsible for periodic gastrointestinal bleeding or even massive and fatal hematemesis. Asymptomatic lesions discovered incidentally during performance of an esophagoscopy should be followed with periodic endoscopy. Those that have bled require treatment, and although resection has been the standard approach, laser endoscopy provides an effective alternative for control of the small bleeding sites visualized through the esophagoscope. Miscellaneous Benign Tumors Benign esophageal tumors other than leiomyomas and polyps are extremely rare. Granular cell myoblastomas actually arise from Schwann cells, not muscle as their name implies. They produce dysphagia, retrosternal pain, nausea, and vomiting. They are difficult to diagnose endoscopically because of their submucosal location and have a characteristic grayish yellow appearance. The overlying mucosa typically shows pseudoepitheliomatous hyperplasia, which may be misdiagnosed histologically as squamous cell carcinoma. Local excision is sufficient treatment of symptomatic tumors. Papillomas, sessile lobulated tumors that have a fibrous core and are covered by squamous mucosa, have been reported. Most occur in association with some degree of esophageal obstruction, most often in the distal esophagus. Papillomas have been postulated to represent localized epithelial hyperplasia or even to be premalignant lesions, but their true significance is unknown. On the basis of their size and radiographic configuration, papillomas at times warrant esophageal exploration to exclude malignancy, but a major resection should be avoided because local excision is adequate therapy. Esophageal adenomas, Carcinoid tumors, and Inflammatory pseudotumors also have been reported but are so rare that they are mentioned only for the sake of completeness.
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Cysts Esophageal cysts arise as outpouchings of the embryonic foregut. The esophageal duplication cyst is a variation of the foregut cyst; it extends along the length of the thoracic esophagus and is lined by squamous epithelium. It has submucosal and muscle layers, the latter of which interdigitate with the outer longitudinal muscle layer of the normal esophagus. Three quarters of esophageal duplication cysts present in childhood, and more than 60% are located along the right side of the esophagus. Esophageal duplication cysts are frequently associated with vertebral anomalies (Klippel-Feil deformity or spina bifida) and spinal cord abnormalities. More than 60% of esophageal cysts cause either respiratory or esophageal symptoms in the first year of life. Those located in the upper third of the esophagus tend to present in infancy, while lower-third cysts may be asymptomatic initially and present later in childhood. Adults present with: dysphagia, choking, or retrosternal pain when previously asymptomatic cysts enlarge as a result of bleeding or infection. In the rare cyst that contains ectopic gastric mucosa, a perforation of the cyst may occur. The diagnosis of an esophageal cyst can usually be made on the basis of its typical radiographic appearance. On the standard posteroanterior chest roentgenogram, the cyst may cause: displacement of the trachea; on lateral chest roentgenogram, it may appear as a retrocardiac posterior mediastinal mass. The barium esophagogram demonstrates a smooth extramucosal esophageal mass that rarely communicates with the esophageal lumen. With computed tomography (CT), may be identified The cystic nature of the lesion and its relation with adjacent mediastinal structures When a duplication cyst is suspected, spinal radiographs should be obtained preoperatively to identify an origin of the cyst in the notochord. Because esophageal cysts have a predilection for bleeding, ulceration, perforation, and infection, excision is generally recommended. This can generally be achieved with low morbidity by an extramucosal resection.
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Esophageal duplication cyst presenting as a high posterior mediastinal mass. (A) Barium esophagogram showing the intramural, extramucosal esophageal mass. (B) CT scan showing the cystic nature of the lesion (arrow).
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Heterotopic Tumors Islets of columnar mucosa may be found lining the pharynx and esophagus. Given the embryologic replacement of the initial columnar ciliated epithelium by stratified squamous epithelium, the occurrence of preserved inlet patches of columnar epithelium is readily explained These islets are much more common near the upper end than the lower end of the esophagus. Endoscopically, they are described as an inlet patch of columnar mucosa. This tissue is not to be confused with Barretts mucosa and has little, if any, premalignant disposition. There have also been isolated reports of sebaceous gland tumors as well as ectopic pancreatic and thyroid tissue within the esophagus. These are primarily autopsy reports that have little clinical significance.
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Squamous Cell Carcinoma World-wide, 95% of all esophageal cancers are squamous cell carcinomas. In the United States and Europe, however, the incidence of adenocarcinoma arising in Barretts mucosa is increasing at an alarming rate and in many areas surpasses that of squamous cell tumors. The incidence of squamous cell carcinoma of the esophagus throughout the world is relatively low 3 or 4 per 100,000 population. This disease occurs most commonly in the seventh decade of life and generally is 1.5 to 3 times more common in men than in women. The cause of esophageal carcinoma is unknown. It is thought to occur most often as a result of prolonged exposure of the esophageal mucosa to noxious stimuli in patients who have a genetic predisposition to the disease: Carcinogenic nitrosamines in the soil, Contamination of foods by mutagenic fungi, Geotrichum candidum, The ingestion of very hot tea Chewing tobacco with or without betel nut, betel leaf, Alcohol consumption and cigarette smoking malnutrition, vitamin deficiencies, anemia, poor oral hygiene, dental caries, previous gastric surgery certain premalignant esophageal conditions
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Pathologically, esophageal carcinoma occurs over a spectrum that ranges from the early lesion, which is limited to the mucosa, to the more advanced form, in which the tumor penetrates the muscle layers of the esophagus or beyond. Carcinoma in situ typically is found in patients between 40 and 50 years of age and gradually progresses to invasive squamous cell carcinoma over 2 to 4 years. Microscopically, early esophageal carcinoma is defined in terms of the depth of tumor involvement, either intraepithelial (carcinoma in situ), intramucosal (limited to the lamina propria), or submucosal. The histologic features of esophageal dysplasia as dysplasia becomes severe, histologic differentiation from carcinoma in situ becomes difficult. Once dysplastic cells are seen traversing the basement membrane and extending into the underlying connective tissue, the diagnosis of early invasion is made. Carcinoma in situ of the esophagus tends to be multifocal. Macroscopic growth patterns: a coarsely granular, reddish, slightly raised, plaque-like type; an erosive type; the occult form, which is not apparent on gross inspection of the esophagus; and the papillary type, in which a slightly polypoid lesion of less than 3 cm is seen. Advanced squamous cell carcinoma of the esophagus is defined as a tumor that involves the muscle layers of the esophagus or beyond. The TNM classification for staging esophageal cancer, divide esophagus into four main sections: the cervical esophagus (from the lower border of the cricoid cartilage to the thoracic inlet, or 15 to 18 cm from the upper incisor teeth); the upper thoracic esophagus (from the thoracic inlet to the level of the carina at about 24 cm at endoscopy); the middle third esophagus (from the carina to half the distance to the esophagogastric junction, or about 32 cm); the lower esophagus (to the esophagogastric junction at 40 cm).
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Using this arbitrary division of the esophagus, 8% of squamous cell carcinomas occur in the cervical esophagus, 55% in the upper and mid-thoracic segments, and 37% in the lower thoracic segment. Macroscopically, 60% of these lesions are fungating intraluminal growths, 25% are ulcerative lesions associated with extensive infiltration of the adjacent esophageal wall, 15% are infiltrating. Microscopically, most squamous cell carcinomas of the esophagus are moderately differentiated and contain islands of atypical squamous cells that infiltrate the underlying adjacent normal tissues and contain keratin pearl formation and intercellular bridges between the tumor cells. Esophageal carcinoma tends to be multifocal, and a patient who survives treatment of one carcinoma has at least twice the risk of developing a second primary esophageal neoplasm. Esophageal carcinoma is notorious for its aggressive biologic behavior. It tends to infiltrate locally, involving adjacent lymph nodes and spreading along the extensive submucosal esophageal lymphatic channels. Lack of an esophageal serosa favors tumor extension into adjacent structures such as the pericardium, aorta, tracheobronchial tree, diaphragm, stomach, and left recurrent laryngeal nerve. Mediastinal, supraclavicular, or celiac lymph node metastases are present in at least 75% of patients with esophageal cancer at the time of initial diagnosis. Cervical esophageal cancers tend to drain to the deep cervical, paraesophageal, posterior mediastinal, and tracheobronchial lymph nodes, while the lower esophageal tumors spread to paraesophageal, celiac, and splenic hilar lymph nodes. Distant spread to the liver and lungs is seen in 90% of cases at autopsy. The prognosis of invasive SCC is dismal, with 5% to 12% of patients surviving 5 years. Unfortunately, extraesophageal tumor extension is present in 70% of cases at the time of diagnosis, and when lymph node metastases are present, 5-year survival is only 3%, compared with 42% when there is no lymph node spread.
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Adenocarcinoma Adenocarcinomas account for 2.5% to 8% of primary esophageal cancers, but the frequency of this tumor is increasing at a rate surpassing that of any other cancer. This increase is the result of the growing prevalence of adenocarcinoma arising in Barretts mucosa. Adenocarcinomas most often involve the distal third of the esophagus, have a peak incidence in the sixth decade of life, and are three times more common in men than in woman. Esophageal adenocarcinoma has three potential origins: The malignant degeneration of metaplastic columnar epithelium (Barretts mucosa), Heterotopic islands of columnar epithelium, or The esophageal submucosal glands. !!! In addition, the esophagus may be involved secondarily by a gastric carcinoma growing upward. Severe gastroesophageal reflux is a major factor in the development of a columnar epitheliumlined (Barretts) esophagus. Refluxed gastric acid, proteases, and bile erode the normal squamous epithelium, and the residual pluripotential basal cells may differentiate along multiple cell lines, producing a variety of columnar epithelial cell types. The diagnosis of Barretts esophagus is established at endoscopy by histologic documentation of columnar mucosa extending into the tubular esophagus at least 2 cm above the anatomic esophagogastric junction. This metaplasia may extend up to the thoracic inlet It has been estimated that patients with Barretts esophagus are 40 times more likely to develop adenocarcinoma than the general population. Barretts mucosa occurs in three characteristic histologic patterns: Gastric fundus-type epithelium, which has a foveolar surface pattern (no villi), but contains glands with parietal cells, chief cells, and mucous cells Junctional-type epithelium, in which there are no villi present and in which cardiac-type mucous glands without parietal or chief cells are seen. The mucosa has a foveolar pattern that is flat and typically is seen in normal colon, gastric cardia, and villous atrophy of the small bowel.
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Specialized columnar epithelium, which is typically characterized by villiform folds lined by a single layer of glycoprotein-secreting columnar cells and mucus-secreting goblet cells. Cryptlike glands between the villi are also lined by columnar and goblet cells and contain few if any parietal or chief cells. This epithelium has also been termed incomplete intestinal metaplasia because only the goblet cell component of intestinal epithelium is present. Dysplasia occurs to varying degrees in Barretts mucosa, and dysplasia clearly is a premalignant esophageal lesion. The histologic features of dysplasia are: an increased nuclear/cytoplasmic ratio, loss of the basilar orientation of the epithelial cells along the basement membrane, irregular chromatin clumping, hyperchromatic nuclei, and prominence of the nucleoli Severe dysplasia is almost always associated with carcinoma in situ and mandates aggressive therapy.
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Esophageal adenocarcinoma has an aggressive biologic behavior that is characterized by frequent transmural invasion and lymphatic spread. Because these tumors arise in the lower third of the esophagus, paraesophageal, celiac axis, and splenic hilum lymph node metastases are common. The lung and liver are the visceral organs most frequently involved by metastases. Esophageal adenocarcinoma is associated with a 5-year survival rate of 0% to 7%. Without lymph node involvement, survival of 5 years is possible, compared with an average survival of only 9 months in patients with lymph node involvement. Other Malignancies Anaplastic small cell (oat cell) carcinoma arises in the esophagus from the same argyrophilic cells that give rise to this tumor in the lung. As is the case with their pulmonary counterparts, these tumors contain neurosecretory granules on electron microscopy. They are extremely aggressive tumors, they are commonly associated with distant spread at the time of diagnosis, and survival beyond 1 year is rare. Adenoid cystic esophageal carcinoma is another rare lesion, and fewer than 50 cases have been reported. These tumors typically occur in the middle third of the esophagus, are discovered late in their course, metastasize widely, and are associated with a median survival of only 9 months. About 100 cases of malignant melanoma of the esophagus have been reported, and these rare lesions constitute less than 0.1% of esophageal malignancies. Malignant melanoma may involve the esophagus either as a primary tumor or as a secondary metastasis. In the former situation, it is thought to arise from melanocytes that occur in the esophagus. These tumors typically present as large (7 cm or more) polypoid masses, which may or may not be pigmented. The average survival is only 13.4 months, and less than 5% survive 5 years. Metastasis to liver, lymph nodes, lung, and brain is common. Carcinosarcoma describes a lesion of the esophagus that has histologic features of both squamous cell carcinoma and malignant spindle cell sarcoma. These typically polypoid tumors generally occur in the distal two thirds of the esophagus, grow to large size (10 to 15 cm), and have a poor prognosis, with 2% to 6% of patients surviving 5 years.
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Local Effects Symptoms from esophageal carcinoma may be insidious in onset: nonspecific retrosternal discomfort, indigestion, or transient dysphagia. Early esophageal carcinoma that is limited to the mucosa or submucosa may be completely asymptomatic or may produce localized spasm that is manifested as periodic esophageal obstruction. Because the esophagus is a distensible tube, a major portion of the circumference must be involved before obstructive symptoms develop. Many patients subconsciously alter their eating habits by eliminating some foods, chewing their food more thoroughly, and using more liquids to wash down food. By the time of presentation to a physician with a complaint of dysphagia, symptoms have often been present for 6 to 8 months. Dysphagia is the most common presenting symptom of esophageal carcinoma. It develops in 90% of patients and is the primary manifestation of the disease in more than 80%. It may be: a subtle retrosternal discomfort as a bolus of food is swallowed, a transient feeling of retrosternal discomfort with swallowing that may not recur for several weeks or months, painful swallowing (odynophagia), complete esophageal obstruction. Weight loss is the next most common symptom and is present in about 40% of patients with esophageal carcinoma. Pain is the initial symptom in 10% of patients. It may be: precordial, retrosternal, epigastric, or intrascapular. Transient retrosternal pain radiating to the back or neck as the solid bolus of food passes through the tumor and causes local distention or muscle contraction has a much different implication than constant, boring retrosternal or epigastric pain, which more often represents local invasion by the tumor.
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Regurgitation of undigested food that has not passed through the esophagus should not be confused with the vomiting of gastric contents. Respiratory symptoms may be due either to aspiration or to direct invasion of the tracheobronchial tree by the tumor. These symptoms include cough, dyspnea, pleuritic pain, or hemoptysis. Hematemesis is a rare, early symptom of esophageal carcinoma, but bleeding from an esophageal malignancy is seldom of sufficient quantity to cause melena. Hoarseness from recurrent laryngeal nerve involvement is an ominous sign of unresectability. The course of the left main-stem bronchus anterior to the esophagus at the level of the carina is significant in the patient with a mid-esophageal tumor because the common wall between the esophagus and left main-stem bronchus may become involved with tumor and lead to the development of a malignant tracheoesophageal fistula. Systemic Effects Although the systemic effects of esophageal carcinoma are less well recognized than the local effects, they may have important clinical significance.
Weight loss and Negative nitrogen balance due to starvation have direct implications on the morbidity and mortality of esophageal resection in these patients. Virtually every patient with advanced esophageal obstruction is Dehydrated and total body volume depleted from impaired oral intake. The patient with esophageal obstruction is prone to the development of Severe hypokalemia with secondary muscle weakness. One to 2 L of saliva is produced each day, and the concentration of potassium within saliva (20 mEq/mL) is higher than that in any other gastrointestinal secretions. Patients who are unable to swallow their saliva, therefore, may present with marked hypokalemia. Fever and systemic toxicity may be due to aspiration from the obstructed esophagus.
The production of parathormone by some squamous cell esophageal carcinomas has been documented and may result in hypercalcemia, even in the absence of bone metastases. Preoperative hypercalcemia in the patient with esophageal carcinoma and no demonstrable bone metastases has been suggested to be a poor prognostic sign. Apparently a vagal nervemediated response, the occurrence of swallow syncope has been reported in a few patients with esophageal obstruction due to carcinoma.
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History and Physical Examination 90% of patients with esophageal carcinoma experience dysphagia as their primary presenting symptom, thus a complaint of dysphagia in any adult 50 years of age or older cannot be taken lightly. A complaint of dysphagia warrants both a barium swallow examination and an endoscopic evaluation to rule out the presence of carcinoma. The combination of esophageal biopsy and brushings for cytologic evaluation establishes a diagnosis of carcinoma in 95% of patients with malignant strictures. Patients with long-standing reflux symptoms that have been well controlled with medical therapy who then develop an increase in retrosternal discomfort should not be presumed to have esophagitis. Rather, they should undergo appropriate radiographic and endoscopic evaluation. Aside from evidence of weight loss, most patients with esophageal carcinoma have few objective findings on physical examination to aid in the diagnosis. Nonetheless, careful examination for cervical or supraclavicular lymph node metastases, abdominal masses, and liver nodularity is warranted. The finding of a hard, supraclavicular lymph node in the patient with an intrathoracic esophageal carcinoma warrants fine-needle aspiration biopsy. If metastatic disease is documented, the presence of a stage IV tumor has been established. Resectional therapy of the esophageal tumor in this situation is seldom justified because the patients expected survival is so poor. Laboratory studies should include a complete blood count, blood urea nitrogen, and serum creatinine to assess the state of hydration, as well as liver function tests, including total protein and albumin levels to assess nutrition. Serum electrolytes, particularly potassium and calcium levels, should also be obtained. In obtaining a history from the patient who complains of dysphagia, the physician should ask the patient to localize with one finger on the anterior chest or neck the point at which food lodges when swallowing. The patient with a mechanical esophageal obstruction such as a carcinoma is able to localize the consistent point of obstruction without difficulty. This is in contrast to the patient with neuromotor obstruction, who may only sense slow esophageal emptying diffusely in the retrosternal area.
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Radiographic Studies A barium swallow examination is the first study that should be obtained in a patient who complains of dysphagia. Tumors of the cervical esophagus are most difficult to identify by barium swallow examination, and carcinoma of the cardia may be confused with achalasia, a benign stricture, or esophageal spasm. The typical esophageal carcinoma presents radiographically as an irregular, rigid narrowing of the esophageal wall. The normal mucosal pattern is frequently destroyed. Polypoid fungating tumors present as irregular filling defects with ulcerated borders within the esophagus. An old dictum relates that an esophagus that is dilated proximal to a stenosis is most indicative of a benign chronic obstruction, whereas an esophagus proximal to a carcinoma has not had enough time to dilate. (This observation has proved to be incorrect on numerous occasions). Similarly, although a smooth, tapered radiographic esophageal stricture supposedly reflects benign disease, any stenosis merits esophageal biopsy and brushings for cytologic evaluation to rule out carcinoma. The barium swallow examination may also show a soft tissue mass adjacent to the esophageal tumor indicative of extraesophageal local invasion. In half of patients with esophageal carcinoma is the plain chest radiograph abnormal, the most common findings being: an airfluid level in the obstructed esophagus, a dilated esophagus, abnormal mediastinal soft tissue representing adenopathy, pleural effusions, or pulmonary metastases.
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(A) Barium esophagogram showing an upper esophageal squamous cell carcinoma at the level of the aortic arch. Note the mucosal irregularity and shelf of tumor, which is characteristic of carcinoma. (B) Esophagogram showing a distal esophageal adenocarcinoma presenting as a characteristic applecore constriction above the esophagogastric junction. 82
The chest and upper abdominal CT scan is the standard radiographic technique for staging esophageal carcinoma. esophageal wall thickness should not exceed 5 mm on CT scanning, regional adenopathy or pulmonary, liver, adrenal, or distant nodal metastasis. CT scan, guided tissue diagnosis with fine-needle aspiration biopsy is warranted. A positive histologic diagnosis of stage IV carcinoma translates to an average survival of only 6 to 12 months, and therefore an operation of the magnitude of esophagectomy is contraindicated. Several investigators have reported the value of CT in evaluating resectability of esophageal carcinoma. Bronchoscopy Bronchoscopy should be performed in patients with carcinoma of the upper and middle thirds of the esophagus to exclude invasion of the posterior membranous trachea or main-stem bronchi, which precludes a safe esophagectomy. Other Studies. Magnetic resonance imaging to evaluate mediastinal invasion has not gained widespread popularity. Bone scan is not warranted unless the patient has specific complaints suggesting that bone metastases exist. routine brain scans are not indicated because brain metastases from carcinoma of the esophagus are uncommon (less than 4% in patients being evaluated for esophagectomy).20
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Esophagoscopy Esophagoscopy is one of the most important diagnostic tools in the assessment of the patient with esophageal symptoms from any cause. The flexible fiberoptic esophagoscope permits endoscopic assessment with greater ease gf obstructing lesions of esophagus Endoscopic Vital Staining, Endoscopic Ultrasound and Endoscopic Abrasive cytology Vital staining of the esophageal mucosa is a technique that is useful in detecting dysplastic esophageal lesions that are not obvious on direct endoscopic assessment. Carcinoma in situ (intraepithelial carcinoma) or microinvasive carcinoma may appear endoscopically as flat, nondescript lesions (leukoplakia or erythroplakia) and therefore can be difficult to diagnose. Lugol (3% iodide) solution or 2% toluidine blue may be applied through the esophagoscope to the esophageal mucosa. Lugol solution stains normal glycogenic esophageal mucosa brown, while abnormal mucosa (early carcinoma, esophagitis, Barretts mucosa) remains unstained. Toluidine blue is a metachromatic stain with affinity for cell nuclei. Therefore, tissues with a high cellular density and high nucleus/cytoplasm ratio take up the stain quickly and retain it for about 1 hour. Endoscopic ultrasound is being used with increasing frequency as an adjunct to the standard radiologic and endoscopic assessment of esophageal disease. It offers the potential for more sensitive staging of esophageal carcinoma by detecting the depth of invasion and the presence of abnormal mediastinal adenopathy. Ultrasound permits the endoscopic delineation of the mucosa, submucosa, and muscular layers of the esophagus as well as adjacent tissues. Lymph nodes as small as 5 mm can be recognized with this instrument. Endoscopic Abrasive cytology using a swallowed balloon catheter (balloon cytology) has been extremely effective in screening for carcinoma Combining abrasive cytology with vital staining of the esophageal mucosa may prove to yield the best sensitivity and specificity for screening populations.
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Premalignant Esophageal Lesions Chronic irritation of esophageal mucosa by a variety of noxious stimuli (alcohol, tobacco, hot foods and liquids) eventually may lead to the development of esophageal carcinoma. A variety of esophageal lesions have a recognized premalignant nature: The premalignant nature of Barretts esophagitis was discussed earlier. Reflux Esophagitis constitutes a chronic chemical injury of the esophageal mucosa, it is regarded as a potentially premalignant abnormality of the esophagus that requires aggressive medical therapy or surgical control. About 10% to 12% of patients with achalasia of cardia who are observed for 15 years or longer develop esophageal carcinoma. The cause is thought to be related to the irritating effects of the fermenting intraesophageal contents on the adjacent esophageal mucosa. Plummer-Vinson syndrome (Paterson-Kelly syndrome or sideropenic dysphagia) is a premalignant esophageal condition. The term sideropenic dysphagia refers to the development of cervical dysphagia in patients who have iron-deficiency anemia. Familial keratosis palmaris et plantaris (tylosis) is associated with an increased incidence of esophageal carcinoma Radiation Esophagitis during the course of treatment for lymphoma, lung, breast, or other mediastinal malignancies are at increased risk for developing esophageal carcinoma years later. Within Esophageal Diverticula several isolated reports have been made of esophageal carcinomas that have been found incidentally presumably as a result of the irritating effects on the mucosa of stagnant, putrefying food within the pouch. Esophageal diverticula are therefore also regarded as premalignant esophageal lesions, although this occurrence is extremely rare.
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Treatment of Esophageal Cancer Therapy of esophageal carcinoma is influenced by the knowledge that in most of these patients, local tumor invasion or distant metastatic disease precludes cure. Neither chemotherapy, radiotherapy, nor surgery alone has achieved significant and consistent long-term survival in patients with esophageal carcinoma. Radiation Although squamous cell carcinoma is generally regarded as a radiosensitive and therefore potentially curable tumor, radiotherapy alone has not achieved cure in most of these patients. Radiotherapy is used in the treatment of esophageal carcinoma to provide either palliation or cure as an adjunct to esophagectomy. Palliative radiotherapy in the range of 4000 to 5000 cGy over 3 to 4 weeks relieves dysphagia sufficiently in nearly half of patients with advanced metastatic carcinoma and severe dysphagia to allow them to swallow liquids and diet supplements. Curative supervoltage radiotherapy is delivered in doses of 5000 to 7000 cGy over 5 to 7 weeks, using rotational and oblique ports to avoid spinal cord injury. Unfortunately, the average 5-year survival after such treatment is between 6% and 10% in most series because radiation alone fails to control either the primary tumor or distant metastatic disease. Thus, reported 5-year survival rates after esophageal resection for carcinoma usually average between 10% and 15%, with more than 80% of patients dying within 1 year of diagnosis. Several Japanese reports indicate 5-year survival rates of 25% to 38%, with combined preoperative radiotherapy followed by resection. Intubation A variety of endoesophageal tubes (Celestin, Fell, Mackler, Mousseau-Barbin, Souttar, Wilson-Cook) have been used to provide palliation in patients with esophageal carcinoma. A variety of expandable intraesophageal metallic stents have been used to achieve palliation in patients with unresectable esophageal carcinoma.26,27 These stents are easier to insert than the older plastic tubes, have a larger lumen, and theoretically, carry less risk of perforation. They are inserted under fluoroscopy using a flexible esophagoscope.
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Laser Endoscopic laser fulgurating of esophageal carcinoma, particularly with the Nd:YAG laser, has been used to achieve temporary relief of the esophageal obstruction in patients with unresectable tumors. Generally, multiple sessions are required to resect sufficient tumor to achieve an adequate lumen, and functional success with restoration of comfortable swallowing is achieved in 75% to 80% of patients. Bypass A variety of surgical procedures, such as substernal gastric or colon bypass, have been developed as palliative internal bypasses of unresectable esophageal carcinomas. This is simply too large an operation for a patient with so advanced a malignancy. Surgical Resection Transthoracic Resection. For most patients with localized esophageal carcinoma, resection provides the most effective and reliable palliation of dysphagia. The traditional surgical approach to distal esophageal carcinoma is a left thoracoabdominal incision (Fig. 1911). After resecting the distal esophagus, proximal stomach, and adjacent lymph nodes, an intrathoracic esophagogastric anastomosis is performed. Tumors involving the mid-esophagus are resected through either a thoracoabdominal or separate thoracic and abdominal incisions, and a high intrathoracic esophagogastric anastomosis is performed (Fig. 19-12). Transhiatal Resection. During the past two decades, the technique of transhiatal esophagectomy without thoracotomy has been popularized as an operation that minimizes the factors responsible for most poor results from traditional transthoracic esophageal resection and reconstruction. In this operation, irrespective of the level of the tumor, the entire intrathoracic esophagus is resected, the stomach is repositioned in the posterior mediastinum in the original esophageal bed, and the gastric fundus is anastomosed to the cervical esophagus above the level of the clavicles.
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Standard thoracoabdominal esophagogastrectomy for carcinomas of the distal esophagus and cardia. (A) Thoracoabdominal incision. (B) Tissue to be resected (colored area). (C) Completed reconstruction after intrathoracic esophagogastric anastomosis
Standard thoracoabdominal esophagogastrectomy for tumors of the upper and middle thirds of the thoracic esophagus. (A) Either the continuous thoracoabdominal incision or separate thoracic and abdominal incisions are used. (B) Portion of esophagus to be resected (colored area). (C) Completed reconstruction with high intrathoracic esophagogastric anastomosis and gastric drainage procedure.
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Transhiatal Esophagectomy Mobilization of the thoracic esophagus from the posterior mediastinum
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This operation has been criticized because of its limited exposure of the intrathoracic esophagus through the diaphragmatic hiatus and, therefore, the risk of intraoperative bleeding from the divided aortic esophageal branches. In addition, one cannot carry out a complete mediastinal lymph node dissection through the diaphragmatic hiatus for purposes of staging or potential cure. Radical Resection. The radical transthoracic esophagectomy with en bloc dissection of contiguous lymph nodebearing tissues for esophageal carcinoma. This is a much more formidable operation, the results of which, when compared with those of transhiatal esophagectomy without thoracotomy and no formal lymph node dissection. As a general rule, the stomach is the preferred visceral esophageal substitute, being far more resilient than intestine and readily reaching to the neck for replacement of the entire esophagus. Colonic interposition is a major operative undertaking in patients with esophageal carcinoma and should be used only in selected cases in which the stomach is not available for esophageal replacement. Multimodality Therapy Efforts have been made to improve survival in patients with esophageal carcinoma by using multimodality therapy in combination with surgery. Combined preoperative chemotherapy and radiotherapy before transhiatal esophagectomy for carcinoma, for example, has provided encouraging survival statistics. They received 3 weeks of chemotherapy with cisplatin, vinblastine, and 5-fluorouracil, concurrent with 3750 to 4500 cGy of radiotherapy. After a 3-week recovery period, transhiatal esophagectomy was accomplished.
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