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Surgery_Schwartz_7202 | Surgery_Schwartz | perforation is the problem. This is due to the stretching of the supradiaphragmatic portion of the gastric wall. In this situation, the hernia sac represents an extension of the abdominal cavity, and the GEJ remains exposed to abdominal pressure.DiagnosisAbnormalities on the chest radiogram can be variable and should not be depended upon to make the diagnosis. This is because the abnormalities are dependent on three factors: (a) the time interval between the perforation and the radiographic examination, (b) the site of perforation, and (c) the integrity of the mediastinal pleura. Mediastinal emphysema, a strong indica-tor of perforation, takes at least 1 hour to be demonstrated and is present in only 40% of patients. Mediastinal widening second-ary to edema may not occur for several hours. The site of perfo-ration also can influence the radiographic findings. In cervical perforation, cervical emphysema is common and mediastinal emphysema rare; the converse is true for thoracic | Surgery_Schwartz. perforation is the problem. This is due to the stretching of the supradiaphragmatic portion of the gastric wall. In this situation, the hernia sac represents an extension of the abdominal cavity, and the GEJ remains exposed to abdominal pressure.DiagnosisAbnormalities on the chest radiogram can be variable and should not be depended upon to make the diagnosis. This is because the abnormalities are dependent on three factors: (a) the time interval between the perforation and the radiographic examination, (b) the site of perforation, and (c) the integrity of the mediastinal pleura. Mediastinal emphysema, a strong indica-tor of perforation, takes at least 1 hour to be demonstrated and is present in only 40% of patients. Mediastinal widening second-ary to edema may not occur for several hours. The site of perfo-ration also can influence the radiographic findings. In cervical perforation, cervical emphysema is common and mediastinal emphysema rare; the converse is true for thoracic |
Surgery_Schwartz_7203 | Surgery_Schwartz | hours. The site of perfo-ration also can influence the radiographic findings. In cervical perforation, cervical emphysema is common and mediastinal emphysema rare; the converse is true for thoracic perforations. Figure 25-73. Barium esophagogram showing a classical, smooth, contoured, punched-out defect of a leiomyoma.Brunicardi_Ch25_p1009-p1098.indd 108301/03/19 6:05 PM 1084SPECIFIC CONSIDERATIONSPART IIFrequently, air will be visible in the erector spinae muscles on a neck radiogram before it can be palpated or seen on a chest radiogram (Fig. 25-74). The integrity of the mediastinal pleura influences the radiographic abnormality in that rupture of the pleura results in a pneumothorax, a finding that is seen in 77% of patients. In two-thirds of patients, the perforation is on the left side; in one-fifth, it is on the right side; and in one-tenth, it is bilateral. If pleural integrity is maintained, mediastinal emphy-sema (rather than a pneumothorax) appears rapidly. A pleural | Surgery_Schwartz. hours. The site of perfo-ration also can influence the radiographic findings. In cervical perforation, cervical emphysema is common and mediastinal emphysema rare; the converse is true for thoracic perforations. Figure 25-73. Barium esophagogram showing a classical, smooth, contoured, punched-out defect of a leiomyoma.Brunicardi_Ch25_p1009-p1098.indd 108301/03/19 6:05 PM 1084SPECIFIC CONSIDERATIONSPART IIFrequently, air will be visible in the erector spinae muscles on a neck radiogram before it can be palpated or seen on a chest radiogram (Fig. 25-74). The integrity of the mediastinal pleura influences the radiographic abnormality in that rupture of the pleura results in a pneumothorax, a finding that is seen in 77% of patients. In two-thirds of patients, the perforation is on the left side; in one-fifth, it is on the right side; and in one-tenth, it is bilateral. If pleural integrity is maintained, mediastinal emphy-sema (rather than a pneumothorax) appears rapidly. A pleural |
Surgery_Schwartz_7204 | Surgery_Schwartz | left side; in one-fifth, it is on the right side; and in one-tenth, it is bilateral. If pleural integrity is maintained, mediastinal emphy-sema (rather than a pneumothorax) appears rapidly. A pleural effusion secondary to inflammation of the mediastinum occurs late. In 9% of patients, the chest radiogram is normal.The diagnosis is confirmed with a contrast esophagram, which will demonstrate extravasation in 90% of patients. The use of a water-soluble medium such as Gastrografin is preferred. Of concern is that there is a 10% false-negative rate. This may be due to obtaining the radiographic study with the patient in the upright position. When the patient is upright, the passage of water-soluble contrast material can be too rapid to demonstrate a small perforation. The studies should be done with the patient in the right lateral decubitus position (Fig. 25-75). In this, the contrast material fills the entire length of the esophagus, allow-ing the actual site of perforation and its | Surgery_Schwartz. left side; in one-fifth, it is on the right side; and in one-tenth, it is bilateral. If pleural integrity is maintained, mediastinal emphy-sema (rather than a pneumothorax) appears rapidly. A pleural effusion secondary to inflammation of the mediastinum occurs late. In 9% of patients, the chest radiogram is normal.The diagnosis is confirmed with a contrast esophagram, which will demonstrate extravasation in 90% of patients. The use of a water-soluble medium such as Gastrografin is preferred. Of concern is that there is a 10% false-negative rate. This may be due to obtaining the radiographic study with the patient in the upright position. When the patient is upright, the passage of water-soluble contrast material can be too rapid to demonstrate a small perforation. The studies should be done with the patient in the right lateral decubitus position (Fig. 25-75). In this, the contrast material fills the entire length of the esophagus, allow-ing the actual site of perforation and its |
Surgery_Schwartz_7205 | Surgery_Schwartz | done with the patient in the right lateral decubitus position (Fig. 25-75). In this, the contrast material fills the entire length of the esophagus, allow-ing the actual site of perforation and its interconnecting cavities to be visualized in almost all patients.ManagementThe key to optimum management is early diagnosis. The most favorable outcome is obtained following primary closure of the perforation within 24 hours, resulting in 80% to 90% survival. Figure 25-76 is an operative photograph taken through a left thoracotomy of an esophageal rupture following a pneumatic dilation for achalasia. The most common location for the injury is the left lateral wall of the esophagus, just above the GEJ. Figure 25-74. Chest radiogram showing air in the deep muscles of the neck following perforation of the esophagus (arrow). This is often the earliest sign of perforation and can be present without evidence of air in the mediastinum.Figure 25-75. Radiographic study of a patient with a | Surgery_Schwartz. done with the patient in the right lateral decubitus position (Fig. 25-75). In this, the contrast material fills the entire length of the esophagus, allow-ing the actual site of perforation and its interconnecting cavities to be visualized in almost all patients.ManagementThe key to optimum management is early diagnosis. The most favorable outcome is obtained following primary closure of the perforation within 24 hours, resulting in 80% to 90% survival. Figure 25-76 is an operative photograph taken through a left thoracotomy of an esophageal rupture following a pneumatic dilation for achalasia. The most common location for the injury is the left lateral wall of the esophagus, just above the GEJ. Figure 25-74. Chest radiogram showing air in the deep muscles of the neck following perforation of the esophagus (arrow). This is often the earliest sign of perforation and can be present without evidence of air in the mediastinum.Figure 25-75. Radiographic study of a patient with a |
Surgery_Schwartz_7206 | Surgery_Schwartz | perforation of the esophagus (arrow). This is often the earliest sign of perforation and can be present without evidence of air in the mediastinum.Figure 25-75. Radiographic study of a patient with a perforation of the esophagus using water-soluble contrast material. The patient is placed in the lateral decubitus position with the left side up to allow complete filling of the esophagus and demonstration of the defect.Figure 25-76. Left thoracotomy in a patient with an esophageal rupture at the gastroesophageal junction following forceful dila-tion of the lower esophagus for achalasia (the surgical clamp is on the stomach, and the Penrose drain encircles the esophagus). The injury consists of a mucosal perforation and extensive splitting of the esophageal muscle from just below the Penrose drain to the stomach.To get adequate exposure of the injury, a dissection similar to that described for esophageal myotomy is performed. A flap of stomach is pulled up and the soiled fat pad at the | Surgery_Schwartz. perforation of the esophagus (arrow). This is often the earliest sign of perforation and can be present without evidence of air in the mediastinum.Figure 25-75. Radiographic study of a patient with a perforation of the esophagus using water-soluble contrast material. The patient is placed in the lateral decubitus position with the left side up to allow complete filling of the esophagus and demonstration of the defect.Figure 25-76. Left thoracotomy in a patient with an esophageal rupture at the gastroesophageal junction following forceful dila-tion of the lower esophagus for achalasia (the surgical clamp is on the stomach, and the Penrose drain encircles the esophagus). The injury consists of a mucosal perforation and extensive splitting of the esophageal muscle from just below the Penrose drain to the stomach.To get adequate exposure of the injury, a dissection similar to that described for esophageal myotomy is performed. A flap of stomach is pulled up and the soiled fat pad at the |
Surgery_Schwartz_7207 | Surgery_Schwartz | drain to the stomach.To get adequate exposure of the injury, a dissection similar to that described for esophageal myotomy is performed. A flap of stomach is pulled up and the soiled fat pad at the GEJ is removed. The edges of the injury are trimmed and closed pri-marily (Fig. 25-77). The closure is reinforced with the use of a pleural patch or construction of a Nissen fundoplication.Mortality associated with immediate closure varies between 8% and 20%. After 24 hours, survival decreases to <50%, and is not influenced by the type of operative therapy (i.e., drainage alone or drainage plus closure of the perforation). If the time delay before closing a perforation approaches 24 hours and the tissues are inflamed, division of the cardia and resection of the diseased portion of the esophagus are recommended. The remainder of the esophagus is mobilized, and as much normal esophagus as pos-sible is saved and brought out as an end cervical esophagostomy. In some situations, the retained | Surgery_Schwartz. drain to the stomach.To get adequate exposure of the injury, a dissection similar to that described for esophageal myotomy is performed. A flap of stomach is pulled up and the soiled fat pad at the GEJ is removed. The edges of the injury are trimmed and closed pri-marily (Fig. 25-77). The closure is reinforced with the use of a pleural patch or construction of a Nissen fundoplication.Mortality associated with immediate closure varies between 8% and 20%. After 24 hours, survival decreases to <50%, and is not influenced by the type of operative therapy (i.e., drainage alone or drainage plus closure of the perforation). If the time delay before closing a perforation approaches 24 hours and the tissues are inflamed, division of the cardia and resection of the diseased portion of the esophagus are recommended. The remainder of the esophagus is mobilized, and as much normal esophagus as pos-sible is saved and brought out as an end cervical esophagostomy. In some situations, the retained |
Surgery_Schwartz_7208 | Surgery_Schwartz | are recommended. The remainder of the esophagus is mobilized, and as much normal esophagus as pos-sible is saved and brought out as an end cervical esophagostomy. In some situations, the retained esophagus may be so long that Brunicardi_Ch25_p1009-p1098.indd 108401/03/19 6:05 PM 1085ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25it loops down into the chest. The contaminated mediastinum is drained and a feeding jejunostomy tube is inserted. The recov-ery from sepsis is often immediate, dramatic, and reflected by a marked improvement in the patient’s condition over a 24-hour period. On recovery from the sepsis, the patient is discharged and returns on a subsequent date for reconstruction with a substernal colon interposition. Failure to apply this aggressive therapy can result in a mortality rate in excess of 50% in patients in whom the diagnosis has been delayed.Nonoperative management of esophageal perforation has been advocated in select situations. The choice of conserva-tive | Surgery_Schwartz. are recommended. The remainder of the esophagus is mobilized, and as much normal esophagus as pos-sible is saved and brought out as an end cervical esophagostomy. In some situations, the retained esophagus may be so long that Brunicardi_Ch25_p1009-p1098.indd 108401/03/19 6:05 PM 1085ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25it loops down into the chest. The contaminated mediastinum is drained and a feeding jejunostomy tube is inserted. The recov-ery from sepsis is often immediate, dramatic, and reflected by a marked improvement in the patient’s condition over a 24-hour period. On recovery from the sepsis, the patient is discharged and returns on a subsequent date for reconstruction with a substernal colon interposition. Failure to apply this aggressive therapy can result in a mortality rate in excess of 50% in patients in whom the diagnosis has been delayed.Nonoperative management of esophageal perforation has been advocated in select situations. The choice of conserva-tive |
Surgery_Schwartz_7209 | Surgery_Schwartz | rate in excess of 50% in patients in whom the diagnosis has been delayed.Nonoperative management of esophageal perforation has been advocated in select situations. The choice of conserva-tive therapy requires skillful judgment and necessitates care-ful radiographic examination of the esophagus. This course of management usually follows an injury occurring during dila-tion of esophageal strictures or pneumatic dilations of achalasia. Conservative management should not be used in patients who have free perforations into the pleural space. Cameron proposed three criteria for the nonoperative management of esophageal perforation: (a) the esophagram must show the perforation to be contained within the mediastinum and drain well back into the esophagus (Fig. 25-78), (b) symptoms should be mild, and (c) there should be minimal evidence of clinical sepsis. If these Figure 25-77. The technique of closure of an esophageal perfora-tion through a left thoracotomy. A. A tongue of stomach is pulled | Surgery_Schwartz. rate in excess of 50% in patients in whom the diagnosis has been delayed.Nonoperative management of esophageal perforation has been advocated in select situations. The choice of conserva-tive therapy requires skillful judgment and necessitates care-ful radiographic examination of the esophagus. This course of management usually follows an injury occurring during dila-tion of esophageal strictures or pneumatic dilations of achalasia. Conservative management should not be used in patients who have free perforations into the pleural space. Cameron proposed three criteria for the nonoperative management of esophageal perforation: (a) the esophagram must show the perforation to be contained within the mediastinum and drain well back into the esophagus (Fig. 25-78), (b) symptoms should be mild, and (c) there should be minimal evidence of clinical sepsis. If these Figure 25-77. The technique of closure of an esophageal perfora-tion through a left thoracotomy. A. A tongue of stomach is pulled |
Surgery_Schwartz_7210 | Surgery_Schwartz | and (c) there should be minimal evidence of clinical sepsis. If these Figure 25-77. The technique of closure of an esophageal perfora-tion through a left thoracotomy. A. A tongue of stomach is pulled up through the esophageal hiatus, and the gastroesophageal fat pad is removed; the edges of the mucosal injury are trimmed and closed using interrupted modified Gambee stitches. B. Reinforcement of the closure with a parietal pleural patch.conditions are met, it is reasonable to treat the patient with hyper-alimentation, antibiotics, and cimetidine to decrease acid secre-tion and diminish pepsin activity. Oral intake is resumed in 7 to 14 days, dependent on subsequent radiographic examinations.MALLORY-WEISS SYNDROMEIn 1929, Mallory and Weiss described four patients with acute upper GI bleeding who were found at autopsy to have mucosal tears at the GEJ. This syndrome, characterized by acute upper GI bleeding following vomiting, is considered to be the cause of up to 15% of all severe | Surgery_Schwartz. and (c) there should be minimal evidence of clinical sepsis. If these Figure 25-77. The technique of closure of an esophageal perfora-tion through a left thoracotomy. A. A tongue of stomach is pulled up through the esophageal hiatus, and the gastroesophageal fat pad is removed; the edges of the mucosal injury are trimmed and closed using interrupted modified Gambee stitches. B. Reinforcement of the closure with a parietal pleural patch.conditions are met, it is reasonable to treat the patient with hyper-alimentation, antibiotics, and cimetidine to decrease acid secre-tion and diminish pepsin activity. Oral intake is resumed in 7 to 14 days, dependent on subsequent radiographic examinations.MALLORY-WEISS SYNDROMEIn 1929, Mallory and Weiss described four patients with acute upper GI bleeding who were found at autopsy to have mucosal tears at the GEJ. This syndrome, characterized by acute upper GI bleeding following vomiting, is considered to be the cause of up to 15% of all severe |
Surgery_Schwartz_7211 | Surgery_Schwartz | who were found at autopsy to have mucosal tears at the GEJ. This syndrome, characterized by acute upper GI bleeding following vomiting, is considered to be the cause of up to 15% of all severe upper GI bleeds. The mechanism is similar to spontaneous esophageal perforation: an acute increase in intra-abdominal pressure against a closed glottis in a patient with a hiatal hernia.Mallory-Weiss tears are characterized by arterial bleeding, which may be massive. Vomiting is not an obligatory factor, as there may be other causes of an acute increase in intra-abdominal pressure, such as paroxysmal coughing, seizures, and retching. The diagnosis requires a high index of suspicion, par-ticularly in the patient who develops upper GI bleeding follow-ing prolonged vomiting or retching. Upper endoscopy confirms the suspicion by identifying one or more longitudinal fissures in the mucosa of the herniated stomach as the source of bleeding.In the majority of patients, the bleeding will stop | Surgery_Schwartz. who were found at autopsy to have mucosal tears at the GEJ. This syndrome, characterized by acute upper GI bleeding following vomiting, is considered to be the cause of up to 15% of all severe upper GI bleeds. The mechanism is similar to spontaneous esophageal perforation: an acute increase in intra-abdominal pressure against a closed glottis in a patient with a hiatal hernia.Mallory-Weiss tears are characterized by arterial bleeding, which may be massive. Vomiting is not an obligatory factor, as there may be other causes of an acute increase in intra-abdominal pressure, such as paroxysmal coughing, seizures, and retching. The diagnosis requires a high index of suspicion, par-ticularly in the patient who develops upper GI bleeding follow-ing prolonged vomiting or retching. Upper endoscopy confirms the suspicion by identifying one or more longitudinal fissures in the mucosa of the herniated stomach as the source of bleeding.In the majority of patients, the bleeding will stop |
Surgery_Schwartz_7212 | Surgery_Schwartz | endoscopy confirms the suspicion by identifying one or more longitudinal fissures in the mucosa of the herniated stomach as the source of bleeding.In the majority of patients, the bleeding will stop sponta-neously with nonoperative management. In addition to blood replacement, the stomach should be decompressed and anti-emetics administered, as a distended stomach and continued vomiting aggravate further bleeding. A Sengstaken-Blakemore tube will not stop the bleeding, as the pressure in the balloon is not sufficient to overcome arterial pressure. Endoscopic injec-tion of epinephrine may be therapeutic if bleeding does not stop spontaneously. Only occasionally will surgery be required to stop blood loss. The procedure consists of laparotomy and high gastrotomy with oversewing of the linear tear. Mortality is uncommon, and recurrence is rare.Figure 25-78. Barium esophagogram showing a stricture and a contained perforation following dilation. The injury meets Cameron criteria: It is | Surgery_Schwartz. endoscopy confirms the suspicion by identifying one or more longitudinal fissures in the mucosa of the herniated stomach as the source of bleeding.In the majority of patients, the bleeding will stop sponta-neously with nonoperative management. In addition to blood replacement, the stomach should be decompressed and anti-emetics administered, as a distended stomach and continued vomiting aggravate further bleeding. A Sengstaken-Blakemore tube will not stop the bleeding, as the pressure in the balloon is not sufficient to overcome arterial pressure. Endoscopic injec-tion of epinephrine may be therapeutic if bleeding does not stop spontaneously. Only occasionally will surgery be required to stop blood loss. The procedure consists of laparotomy and high gastrotomy with oversewing of the linear tear. Mortality is uncommon, and recurrence is rare.Figure 25-78. Barium esophagogram showing a stricture and a contained perforation following dilation. The injury meets Cameron criteria: It is |
Surgery_Schwartz_7213 | Surgery_Schwartz | tear. Mortality is uncommon, and recurrence is rare.Figure 25-78. Barium esophagogram showing a stricture and a contained perforation following dilation. The injury meets Cameron criteria: It is contained within the mediastinum and drawn back into the esophagus, the patient had mild symptoms, and there was no evidence of clinical sepsis. Nonoperative management was successful.Brunicardi_Ch25_p1009-p1098.indd 108501/03/19 6:05 PM 1086SPECIFIC CONSIDERATIONSPART IITable 25-16Endoscopic grading of corrosive esophageal and gastric burnsFirst degree: Mucosal hyperemia and edemaSecond degree: Limited hemorrhage, exudate ulceration, and pseudomembrane formationThird degree: Sloughing of mucosa, deep ulcers, massive hemorrhage, complete obstruction of lumen by edema, charring, and perforationTable 25-17Location of caustic injury (n = 62)Pharynx10%Esophagus70% Upper15% Middle65% Lower2% Whole18%Stomach20% Antral91% Whole9%Both stomach and esophagus14%CAUSTIC INJURYAccidental caustic | Surgery_Schwartz. tear. Mortality is uncommon, and recurrence is rare.Figure 25-78. Barium esophagogram showing a stricture and a contained perforation following dilation. The injury meets Cameron criteria: It is contained within the mediastinum and drawn back into the esophagus, the patient had mild symptoms, and there was no evidence of clinical sepsis. Nonoperative management was successful.Brunicardi_Ch25_p1009-p1098.indd 108501/03/19 6:05 PM 1086SPECIFIC CONSIDERATIONSPART IITable 25-16Endoscopic grading of corrosive esophageal and gastric burnsFirst degree: Mucosal hyperemia and edemaSecond degree: Limited hemorrhage, exudate ulceration, and pseudomembrane formationThird degree: Sloughing of mucosa, deep ulcers, massive hemorrhage, complete obstruction of lumen by edema, charring, and perforationTable 25-17Location of caustic injury (n = 62)Pharynx10%Esophagus70% Upper15% Middle65% Lower2% Whole18%Stomach20% Antral91% Whole9%Both stomach and esophagus14%CAUSTIC INJURYAccidental caustic |
Surgery_Schwartz_7214 | Surgery_Schwartz | 25-17Location of caustic injury (n = 62)Pharynx10%Esophagus70% Upper15% Middle65% Lower2% Whole18%Stomach20% Antral91% Whole9%Both stomach and esophagus14%CAUSTIC INJURYAccidental caustic lesions occur mainly in children, and, in general, rather small quantities of caustics are taken. In adults or teenagers, the swallowing of caustic liquids is usually deliberate, during a suicide attempt, and greater quantities are swallowed. Alkalis are more frequently swallowed accidentally than acids, because strong acids cause an immediate burning pain in the mouth.PathologyThe swallowing of caustic substances causes an acute and a chronic injury. During the acute phase, care focuses on con-trolling the immediate tissue injury and the potential for per-foration. During the chronic phase, the focus is on treatment of strictures and disturbances in pharyngeal swallowing. In the acute phase, the degree and extent of the lesion are dependent on several factors: the nature of the caustic substance, | Surgery_Schwartz. 25-17Location of caustic injury (n = 62)Pharynx10%Esophagus70% Upper15% Middle65% Lower2% Whole18%Stomach20% Antral91% Whole9%Both stomach and esophagus14%CAUSTIC INJURYAccidental caustic lesions occur mainly in children, and, in general, rather small quantities of caustics are taken. In adults or teenagers, the swallowing of caustic liquids is usually deliberate, during a suicide attempt, and greater quantities are swallowed. Alkalis are more frequently swallowed accidentally than acids, because strong acids cause an immediate burning pain in the mouth.PathologyThe swallowing of caustic substances causes an acute and a chronic injury. During the acute phase, care focuses on con-trolling the immediate tissue injury and the potential for per-foration. During the chronic phase, the focus is on treatment of strictures and disturbances in pharyngeal swallowing. In the acute phase, the degree and extent of the lesion are dependent on several factors: the nature of the caustic substance, |
Surgery_Schwartz_7215 | Surgery_Schwartz | is on treatment of strictures and disturbances in pharyngeal swallowing. In the acute phase, the degree and extent of the lesion are dependent on several factors: the nature of the caustic substance, its con-centration, the quantity swallowed, and the time the substance is in contact with the tissues.Acids and alkalis affect tissue in different ways. Alkalis dissolve tissue, and therefore penetrate more deeply, while acids cause a coagulative necrosis that limits their penetration. Animal experiments have shown that there is a correlation between the depth of the lesion and the concentration of sodium hydroxide solution. When a solution of 3.8% comes into contact with the esophagus for 10 seconds, it causes necrosis of the mucosa and the submucosa but spares the muscular layer. A concentration of 22.5% penetrates the whole esophageal wall and into the periesophageal tissues. Cleansing products can contain up to 90% sodium hydroxide. The strength of esophageal contractions varies | Surgery_Schwartz. is on treatment of strictures and disturbances in pharyngeal swallowing. In the acute phase, the degree and extent of the lesion are dependent on several factors: the nature of the caustic substance, its con-centration, the quantity swallowed, and the time the substance is in contact with the tissues.Acids and alkalis affect tissue in different ways. Alkalis dissolve tissue, and therefore penetrate more deeply, while acids cause a coagulative necrosis that limits their penetration. Animal experiments have shown that there is a correlation between the depth of the lesion and the concentration of sodium hydroxide solution. When a solution of 3.8% comes into contact with the esophagus for 10 seconds, it causes necrosis of the mucosa and the submucosa but spares the muscular layer. A concentration of 22.5% penetrates the whole esophageal wall and into the periesophageal tissues. Cleansing products can contain up to 90% sodium hydroxide. The strength of esophageal contractions varies |
Surgery_Schwartz_7216 | Surgery_Schwartz | of 22.5% penetrates the whole esophageal wall and into the periesophageal tissues. Cleansing products can contain up to 90% sodium hydroxide. The strength of esophageal contractions varies according to the level of the esophagus, being weakest at the striated muscle–smooth muscle interface. Consequently, clearance from this area may be somewhat slower, allowing caustic substances to remain in contact with the mucosa longer. This explains why the esophagus is preferentially and more severely affected at this level than in the lower portions.The lesions caused by lye injury occur in three phases. First is the acute necrotic phase, lasting 1 to 4 days after injury. During this period, coagulation of intracellular proteins results in cell necrosis, and the living tissue surrounding the area of necrosis develops an intense inflammatory reaction. Second is the ulcer-ation and granulation phase, starting 3 to 5 days after injury. During this period, the superficial necrotic tissue sloughs, | Surgery_Schwartz. of 22.5% penetrates the whole esophageal wall and into the periesophageal tissues. Cleansing products can contain up to 90% sodium hydroxide. The strength of esophageal contractions varies according to the level of the esophagus, being weakest at the striated muscle–smooth muscle interface. Consequently, clearance from this area may be somewhat slower, allowing caustic substances to remain in contact with the mucosa longer. This explains why the esophagus is preferentially and more severely affected at this level than in the lower portions.The lesions caused by lye injury occur in three phases. First is the acute necrotic phase, lasting 1 to 4 days after injury. During this period, coagulation of intracellular proteins results in cell necrosis, and the living tissue surrounding the area of necrosis develops an intense inflammatory reaction. Second is the ulcer-ation and granulation phase, starting 3 to 5 days after injury. During this period, the superficial necrotic tissue sloughs, |
Surgery_Schwartz_7217 | Surgery_Schwartz | of necrosis develops an intense inflammatory reaction. Second is the ulcer-ation and granulation phase, starting 3 to 5 days after injury. During this period, the superficial necrotic tissue sloughs, leav-ing an ulcerated, acutely inflamed base, and granulation tissue fills the defect left by the sloughed mucosa. This phase lasts 10 to 12 days, and it is during this period that the esophagus is the weakest. Third is the phase of cicatrization and scarring, which begins the third week following injury. During this period, the previously formed connective tissue begins to contract, result-ing in narrowing of the esophagus. Adhesions between granulat-ing areas occur, resulting in pockets and bands. It is during this period that efforts must be made to reduce stricture formation.Clinical ManifestationsThe clinical picture of an esophageal burn is determined by the degree and extent of the lesion. In the initial phase, complaints consist of pain in the mouth and substernal region, | Surgery_Schwartz. of necrosis develops an intense inflammatory reaction. Second is the ulcer-ation and granulation phase, starting 3 to 5 days after injury. During this period, the superficial necrotic tissue sloughs, leav-ing an ulcerated, acutely inflamed base, and granulation tissue fills the defect left by the sloughed mucosa. This phase lasts 10 to 12 days, and it is during this period that the esophagus is the weakest. Third is the phase of cicatrization and scarring, which begins the third week following injury. During this period, the previously formed connective tissue begins to contract, result-ing in narrowing of the esophagus. Adhesions between granulat-ing areas occur, resulting in pockets and bands. It is during this period that efforts must be made to reduce stricture formation.Clinical ManifestationsThe clinical picture of an esophageal burn is determined by the degree and extent of the lesion. In the initial phase, complaints consist of pain in the mouth and substernal region, |
Surgery_Schwartz_7218 | Surgery_Schwartz | ManifestationsThe clinical picture of an esophageal burn is determined by the degree and extent of the lesion. In the initial phase, complaints consist of pain in the mouth and substernal region, hypersali-vation, pain on swallowing, and dysphagia. The presence of fever is strongly correlated with the presence of an esopha-geal lesion. Bleeding can occur, and, frequently, the patient vomits. These initial complaints disappear during the quiescent period of ulceration and granulation. During the cicatrization and scarring phase, the complaint of dysphagia reappears and is due to fibrosis and retraction, resulting in narrowing of the esophagus. Of the patients who develop strictures, 60% do so within 1 month, and 80% within 2 months. If dysphagia does not develop within 8 months, it is unlikely that a stricture will occur. Serious systemic reactions such as hypovolemia and acidosis resulting in renal damage can occur in cases in which the burns have been caused by strong acids. | Surgery_Schwartz. ManifestationsThe clinical picture of an esophageal burn is determined by the degree and extent of the lesion. In the initial phase, complaints consist of pain in the mouth and substernal region, hypersali-vation, pain on swallowing, and dysphagia. The presence of fever is strongly correlated with the presence of an esopha-geal lesion. Bleeding can occur, and, frequently, the patient vomits. These initial complaints disappear during the quiescent period of ulceration and granulation. During the cicatrization and scarring phase, the complaint of dysphagia reappears and is due to fibrosis and retraction, resulting in narrowing of the esophagus. Of the patients who develop strictures, 60% do so within 1 month, and 80% within 2 months. If dysphagia does not develop within 8 months, it is unlikely that a stricture will occur. Serious systemic reactions such as hypovolemia and acidosis resulting in renal damage can occur in cases in which the burns have been caused by strong acids. |
Surgery_Schwartz_7219 | Surgery_Schwartz | is unlikely that a stricture will occur. Serious systemic reactions such as hypovolemia and acidosis resulting in renal damage can occur in cases in which the burns have been caused by strong acids. Respiratory com-plications such as laryngospasm, laryngoedema, and occasion-ally pulmonary edema can occur, especially when strong acids are aspirated.Inspection of the oral cavity and pharynx can indicate that caustic substances were swallowed, but does not reveal that the esophagus has been burned. Conversely, esophageal burns can be present without apparent oral injuries. Because of this poor correlation, early esophagoscopy is advocated to establish the presence of an esophageal injury. To lessen the chance of perfo-ration, the scope should not be introduced beyond the proximal esophageal lesion. The degree of injury can be graded according to the criteria listed in Table 25-16. Even if the esophagoscopy is normal, strictures may appear later. Radiographic examina-tion is not a | Surgery_Schwartz. is unlikely that a stricture will occur. Serious systemic reactions such as hypovolemia and acidosis resulting in renal damage can occur in cases in which the burns have been caused by strong acids. Respiratory com-plications such as laryngospasm, laryngoedema, and occasion-ally pulmonary edema can occur, especially when strong acids are aspirated.Inspection of the oral cavity and pharynx can indicate that caustic substances were swallowed, but does not reveal that the esophagus has been burned. Conversely, esophageal burns can be present without apparent oral injuries. Because of this poor correlation, early esophagoscopy is advocated to establish the presence of an esophageal injury. To lessen the chance of perfo-ration, the scope should not be introduced beyond the proximal esophageal lesion. The degree of injury can be graded according to the criteria listed in Table 25-16. Even if the esophagoscopy is normal, strictures may appear later. Radiographic examina-tion is not a |
Surgery_Schwartz_7220 | Surgery_Schwartz | lesion. The degree of injury can be graded according to the criteria listed in Table 25-16. Even if the esophagoscopy is normal, strictures may appear later. Radiographic examina-tion is not a reliable means to identify the presence of early esophageal injury, but it is important in later follow-up to iden-tify strictures. The most common locations of caustic injuries are shown in Table 25-17.TreatmentTreatment of a caustic lesion of the esophagus is directed toward management of both the immediate and late consequences of the injury. The immediate treatment consists of limiting the burn by administering neutralizing agents. To be effective, this must be done within the first hour. Lye or other alkali can be neutralized with half-strength vinegar, lemon juice, or orange juice. Acid can be neutralized with milk, egg white, or antacids. Sodium bicarbonate is not used because it generates carbon dioxide, Brunicardi_Ch25_p1009-p1098.indd 108601/03/19 6:05 PM 1087ESOPHAGUS AND | Surgery_Schwartz. lesion. The degree of injury can be graded according to the criteria listed in Table 25-16. Even if the esophagoscopy is normal, strictures may appear later. Radiographic examina-tion is not a reliable means to identify the presence of early esophageal injury, but it is important in later follow-up to iden-tify strictures. The most common locations of caustic injuries are shown in Table 25-17.TreatmentTreatment of a caustic lesion of the esophagus is directed toward management of both the immediate and late consequences of the injury. The immediate treatment consists of limiting the burn by administering neutralizing agents. To be effective, this must be done within the first hour. Lye or other alkali can be neutralized with half-strength vinegar, lemon juice, or orange juice. Acid can be neutralized with milk, egg white, or antacids. Sodium bicarbonate is not used because it generates carbon dioxide, Brunicardi_Ch25_p1009-p1098.indd 108601/03/19 6:05 PM 1087ESOPHAGUS AND |
Surgery_Schwartz_7221 | Surgery_Schwartz | can be neutralized with milk, egg white, or antacids. Sodium bicarbonate is not used because it generates carbon dioxide, Brunicardi_Ch25_p1009-p1098.indd 108601/03/19 6:05 PM 1087ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25which might increase the danger of perforation. Emetics are contraindicated because vomiting renews the contact of the caustic substance with the esophagus and can contribute to perforation if too forceful. Hypovolemia is corrected, and broad-spectrum antibiotics are administered to lessen the inflammatory reaction and prevent infectious complications. If necessary, a feeding jejunostomy tube is inserted to provide nutrition. Oral feeding can be started when the dysphagia of the initial phase has regressed.In the past, surgeons waited until the appearance of a stric-ture before starting treatment. Currently, dilations are started the first day after the injury, with the aim of preserving the esophageal lumen by removing the adhesions that occurred in the | Surgery_Schwartz. can be neutralized with milk, egg white, or antacids. Sodium bicarbonate is not used because it generates carbon dioxide, Brunicardi_Ch25_p1009-p1098.indd 108601/03/19 6:05 PM 1087ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25which might increase the danger of perforation. Emetics are contraindicated because vomiting renews the contact of the caustic substance with the esophagus and can contribute to perforation if too forceful. Hypovolemia is corrected, and broad-spectrum antibiotics are administered to lessen the inflammatory reaction and prevent infectious complications. If necessary, a feeding jejunostomy tube is inserted to provide nutrition. Oral feeding can be started when the dysphagia of the initial phase has regressed.In the past, surgeons waited until the appearance of a stric-ture before starting treatment. Currently, dilations are started the first day after the injury, with the aim of preserving the esophageal lumen by removing the adhesions that occurred in the |
Surgery_Schwartz_7222 | Surgery_Schwartz | a stric-ture before starting treatment. Currently, dilations are started the first day after the injury, with the aim of preserving the esophageal lumen by removing the adhesions that occurred in the injured segments. However, this approach is controversial in that dilations can traumatize the esophagus, causing bleed-ing, and perforation, and there are data indicating that exces-sive dilations cause increased fibrosis secondary to the added trauma. The use of steroids to limit fibrosis has been shown to be effective in animals, but their effectiveness in human beings has not been established.Extensive necrosis of the esophagus frequently leads to perforation, and it is best managed by resection. When there is extensive gastric involvement, the esophagus is nearly always necrotic or severely burned, and total gastrectomy and near-total esophagectomy are necessary. The presence of air in the esopha-geal wall is a sign of muscle necrosis and impending perforation and is a strong | Surgery_Schwartz. a stric-ture before starting treatment. Currently, dilations are started the first day after the injury, with the aim of preserving the esophageal lumen by removing the adhesions that occurred in the injured segments. However, this approach is controversial in that dilations can traumatize the esophagus, causing bleed-ing, and perforation, and there are data indicating that exces-sive dilations cause increased fibrosis secondary to the added trauma. The use of steroids to limit fibrosis has been shown to be effective in animals, but their effectiveness in human beings has not been established.Extensive necrosis of the esophagus frequently leads to perforation, and it is best managed by resection. When there is extensive gastric involvement, the esophagus is nearly always necrotic or severely burned, and total gastrectomy and near-total esophagectomy are necessary. The presence of air in the esopha-geal wall is a sign of muscle necrosis and impending perforation and is a strong |
Surgery_Schwartz_7223 | Surgery_Schwartz | severely burned, and total gastrectomy and near-total esophagectomy are necessary. The presence of air in the esopha-geal wall is a sign of muscle necrosis and impending perforation and is a strong indication for esophagectomy.Management of acute injury is summarized in the algo-rithm in Fig. 25-79. Some authors have advocated the use of an intraluminal esophageal stent (Fig. 25-80) in patients who are operated on and found to have no evidence of extensive esophagogastric necrosis. In these patients, a biopsy of the posterior gastric wall should be performed to exclude occult injury. If, histologically, there is a question of viability, a second-look operation should be done within 36 hours. If a stent is inserted, it should be kept in position for 21 days, and removed after a satisfactory barium esophagogram. Esopha-goscopy should be done, and if strictures are present, dilations initiated.Once the acute phase has passed, attention is turned to the prevention and management of | Surgery_Schwartz. severely burned, and total gastrectomy and near-total esophagectomy are necessary. The presence of air in the esopha-geal wall is a sign of muscle necrosis and impending perforation and is a strong indication for esophagectomy.Management of acute injury is summarized in the algo-rithm in Fig. 25-79. Some authors have advocated the use of an intraluminal esophageal stent (Fig. 25-80) in patients who are operated on and found to have no evidence of extensive esophagogastric necrosis. In these patients, a biopsy of the posterior gastric wall should be performed to exclude occult injury. If, histologically, there is a question of viability, a second-look operation should be done within 36 hours. If a stent is inserted, it should be kept in position for 21 days, and removed after a satisfactory barium esophagogram. Esopha-goscopy should be done, and if strictures are present, dilations initiated.Once the acute phase has passed, attention is turned to the prevention and management of |
Surgery_Schwartz_7224 | Surgery_Schwartz | barium esophagogram. Esopha-goscopy should be done, and if strictures are present, dilations initiated.Once the acute phase has passed, attention is turned to the prevention and management of strictures. Both antegrade dilation with a Hurst or Maloney bougie and retrograde dila-tion with a Tucker bougie have been satisfactory. In a series of 1079 patients, early dilations started during the acute phase gave excellent results in 78%, good results in 13%, and poor results in 2%. During the treatment, 55 patients died. In contrast, of 333 patients whose strictures were dilated when they became symptomatic, only 21% had excellent results, 46% good, and 6% poor, with three dying during the process. The length of time the surgeon should persist with dilation before consideration of esophageal resection is problematic. An adequate lumen should be re-established within 6 months to 1 year, with progressively longer intervals between dilations. If, during the course of treat-ment, an adequate | Surgery_Schwartz. barium esophagogram. Esopha-goscopy should be done, and if strictures are present, dilations initiated.Once the acute phase has passed, attention is turned to the prevention and management of strictures. Both antegrade dilation with a Hurst or Maloney bougie and retrograde dila-tion with a Tucker bougie have been satisfactory. In a series of 1079 patients, early dilations started during the acute phase gave excellent results in 78%, good results in 13%, and poor results in 2%. During the treatment, 55 patients died. In contrast, of 333 patients whose strictures were dilated when they became symptomatic, only 21% had excellent results, 46% good, and 6% poor, with three dying during the process. The length of time the surgeon should persist with dilation before consideration of esophageal resection is problematic. An adequate lumen should be re-established within 6 months to 1 year, with progressively longer intervals between dilations. If, during the course of treat-ment, an adequate |
Surgery_Schwartz_7225 | Surgery_Schwartz | resection is problematic. An adequate lumen should be re-established within 6 months to 1 year, with progressively longer intervals between dilations. If, during the course of treat-ment, an adequate lumen cannot be established or maintained (i.e., smaller bougies must be used), operative intervention should be considered. Surgical intervention is indicated when there is (a) complete stenosis in which all attempts from above and below have failed to establish a lumen, (b) marked irregu-larity and pocketing on barium swallow, (c) the development of a severe periesophageal reaction or mediastinitis with dilatation, (d) a fistula, (e) the inability to dilate or maintain the lumen above a 40F bougie, or (f) a patient who is unwilling or unable to undergo prolonged periods of dilation.Ingestion of caustic agentObservation24–48 hoursExploratorylaparotomySecond lookat 36 hoursIntraluminal esophageal stentPosterior gastric wall biopsyJejunostomy1° burn2° & 3° burnEsophagogastric | Surgery_Schwartz. resection is problematic. An adequate lumen should be re-established within 6 months to 1 year, with progressively longer intervals between dilations. If, during the course of treat-ment, an adequate lumen cannot be established or maintained (i.e., smaller bougies must be used), operative intervention should be considered. Surgical intervention is indicated when there is (a) complete stenosis in which all attempts from above and below have failed to establish a lumen, (b) marked irregu-larity and pocketing on barium swallow, (c) the development of a severe periesophageal reaction or mediastinitis with dilatation, (d) a fistula, (e) the inability to dilate or maintain the lumen above a 40F bougie, or (f) a patient who is unwilling or unable to undergo prolonged periods of dilation.Ingestion of caustic agentObservation24–48 hoursExploratorylaparotomySecond lookat 36 hoursIntraluminal esophageal stentPosterior gastric wall biopsyJejunostomy1° burn2° & 3° burnEsophagogastric |
Surgery_Schwartz_7226 | Surgery_Schwartz | of caustic agentObservation24–48 hoursExploratorylaparotomySecond lookat 36 hoursIntraluminal esophageal stentPosterior gastric wall biopsyJejunostomy1° burn2° & 3° burnEsophagogastric resectionCervical esophagostomyJejunostomyResection of adjacent involved organsFull thicknessnecrosisof esophagusand stomachViableesophagusandstomachQuestionableesophagusandstomach Esophagoscopy(Within 12 hours)Figure 25-79. Algorithm summarizing the management of acute caustic injury.Figure 25-80. The use of an esophageal stent to prevent stricture. The stent is constructed from a chest tube and placed in the esopha-gus at the time of an exploratory laparotomy. A Penrose drain is placed over the distal end as a flap valve to prevent reflux. The stent is supported at its upper end by attaching it to a suction catheter that is secured to the nares. Continuous suction removes saliva and mucus trapped in the pharynx and upper esophagus.Brunicardi_Ch25_p1009-p1098.indd 108701/03/19 6:05 PM 1088SPECIFIC | Surgery_Schwartz. of caustic agentObservation24–48 hoursExploratorylaparotomySecond lookat 36 hoursIntraluminal esophageal stentPosterior gastric wall biopsyJejunostomy1° burn2° & 3° burnEsophagogastric resectionCervical esophagostomyJejunostomyResection of adjacent involved organsFull thicknessnecrosisof esophagusand stomachViableesophagusandstomachQuestionableesophagusandstomach Esophagoscopy(Within 12 hours)Figure 25-79. Algorithm summarizing the management of acute caustic injury.Figure 25-80. The use of an esophageal stent to prevent stricture. The stent is constructed from a chest tube and placed in the esopha-gus at the time of an exploratory laparotomy. A Penrose drain is placed over the distal end as a flap valve to prevent reflux. The stent is supported at its upper end by attaching it to a suction catheter that is secured to the nares. Continuous suction removes saliva and mucus trapped in the pharynx and upper esophagus.Brunicardi_Ch25_p1009-p1098.indd 108701/03/19 6:05 PM 1088SPECIFIC |
Surgery_Schwartz_7227 | Surgery_Schwartz | catheter that is secured to the nares. Continuous suction removes saliva and mucus trapped in the pharynx and upper esophagus.Brunicardi_Ch25_p1009-p1098.indd 108701/03/19 6:05 PM 1088SPECIFIC CONSIDERATIONSPART IIThe variety of abnormalities seen requires that creativity be used when considering esophageal reconstruction. Skin tube esophagoplasties are now used much less frequently than they were in the past, and are mainly of historical interest. Currently, the stomach, jejunum, and colon are the organs used to replace the esophagus, through either the posterior mediastinum or the retrosternal route. A retrosternal route is chosen when there has been a previous esophagectomy or there is extensive fibrosis in the posterior mediastinum. When all factors are considered, the order of preference for an esophageal substitute is (a) colon, (b) stomach, and (c) jejunum. Free jejunal grafts based on the supe-rior thyroid artery have provided excellent results. Whatever method is | Surgery_Schwartz. catheter that is secured to the nares. Continuous suction removes saliva and mucus trapped in the pharynx and upper esophagus.Brunicardi_Ch25_p1009-p1098.indd 108701/03/19 6:05 PM 1088SPECIFIC CONSIDERATIONSPART IIThe variety of abnormalities seen requires that creativity be used when considering esophageal reconstruction. Skin tube esophagoplasties are now used much less frequently than they were in the past, and are mainly of historical interest. Currently, the stomach, jejunum, and colon are the organs used to replace the esophagus, through either the posterior mediastinum or the retrosternal route. A retrosternal route is chosen when there has been a previous esophagectomy or there is extensive fibrosis in the posterior mediastinum. When all factors are considered, the order of preference for an esophageal substitute is (a) colon, (b) stomach, and (c) jejunum. Free jejunal grafts based on the supe-rior thyroid artery have provided excellent results. Whatever method is |
Surgery_Schwartz_7228 | Surgery_Schwartz | of preference for an esophageal substitute is (a) colon, (b) stomach, and (c) jejunum. Free jejunal grafts based on the supe-rior thyroid artery have provided excellent results. Whatever method is selected, it must be emphasized that these procedures cannot be taken lightly; minor errors of judgment or technique may lead to serious or even fatal complications.Critical in the planning of the operation is the selection of cervical esophagus, pyriform sinus, or posterior pharynx as the site for proximal anastomosis. The site of the upper anastomosis depends on the extent of the pharyngeal and cervical esophageal damage encountered. When the cervical esophagus is destroyed and a pyriform sinus remains open the anastomosis can be made to the hypopharynx (Fig. 25-81). When the pyriform sinuses are completely stenosed, a transglottic approach is used to perform an anastomosis to the posterior oropharyngeal wall (Fig. 25-82). This allows excision of supraglottic strictures and elevation and | Surgery_Schwartz. of preference for an esophageal substitute is (a) colon, (b) stomach, and (c) jejunum. Free jejunal grafts based on the supe-rior thyroid artery have provided excellent results. Whatever method is selected, it must be emphasized that these procedures cannot be taken lightly; minor errors of judgment or technique may lead to serious or even fatal complications.Critical in the planning of the operation is the selection of cervical esophagus, pyriform sinus, or posterior pharynx as the site for proximal anastomosis. The site of the upper anastomosis depends on the extent of the pharyngeal and cervical esophageal damage encountered. When the cervical esophagus is destroyed and a pyriform sinus remains open the anastomosis can be made to the hypopharynx (Fig. 25-81). When the pyriform sinuses are completely stenosed, a transglottic approach is used to perform an anastomosis to the posterior oropharyngeal wall (Fig. 25-82). This allows excision of supraglottic strictures and elevation and |
Surgery_Schwartz_7229 | Surgery_Schwartz | are completely stenosed, a transglottic approach is used to perform an anastomosis to the posterior oropharyngeal wall (Fig. 25-82). This allows excision of supraglottic strictures and elevation and anterior tilting of the larynx. In both of these situations, the patient must relearn to swallow. Recovery is long and difficult and may require several endoscopic dilations—and often reop-erations. Sleeve resections of short strictures are not successful because the extent of damage to the wall of the esophagus can be greater than realized, and almost invariably the anastomosis is carried out in a diseased area.The management of a bypassed damaged esophagus after injury is problematic. If the esophagus is left in place, ulcer-ation from gastroesophageal reflux or the development of carcinoma must be considered. The extensive dissection neces-sary to remove the esophagus, particularly in the presence of marked periesophagitis, is associated with significant morbidity. Leaving the esophagus | Surgery_Schwartz. are completely stenosed, a transglottic approach is used to perform an anastomosis to the posterior oropharyngeal wall (Fig. 25-82). This allows excision of supraglottic strictures and elevation and anterior tilting of the larynx. In both of these situations, the patient must relearn to swallow. Recovery is long and difficult and may require several endoscopic dilations—and often reop-erations. Sleeve resections of short strictures are not successful because the extent of damage to the wall of the esophagus can be greater than realized, and almost invariably the anastomosis is carried out in a diseased area.The management of a bypassed damaged esophagus after injury is problematic. If the esophagus is left in place, ulcer-ation from gastroesophageal reflux or the development of carcinoma must be considered. The extensive dissection neces-sary to remove the esophagus, particularly in the presence of marked periesophagitis, is associated with significant morbidity. Leaving the esophagus |
Surgery_Schwartz_7230 | Surgery_Schwartz | be considered. The extensive dissection neces-sary to remove the esophagus, particularly in the presence of marked periesophagitis, is associated with significant morbidity. Leaving the esophagus in place preserves the function of the Figure 25-82. Anastomosis of the bowel to the posterior orophar-ynx. The anastomosis is done through an inverted trapezoid incision above the thyroid cartilage (dotted line). A triangle-shaped piece of the upper half of the cartilage is resected. Closure of the oropharynx is done so that the larynx is pulled up (sagittal section).Figure 25-81. Anastomosis of the bowel to a preserved pyriform sinus. To identify the site, a finger is inserted into the free pyriform sinus through a suprahyoid incision (dotted line). This requires removing the lateral inferior portion of the thyroid cartilage as shown in cross-section.vagus nerves, and, in turn, the function of the stomach. On the other hand, leaving a damaged esophagus in place can result in multiple blind | Surgery_Schwartz. be considered. The extensive dissection neces-sary to remove the esophagus, particularly in the presence of marked periesophagitis, is associated with significant morbidity. Leaving the esophagus in place preserves the function of the Figure 25-82. Anastomosis of the bowel to the posterior orophar-ynx. The anastomosis is done through an inverted trapezoid incision above the thyroid cartilage (dotted line). A triangle-shaped piece of the upper half of the cartilage is resected. Closure of the oropharynx is done so that the larynx is pulled up (sagittal section).Figure 25-81. Anastomosis of the bowel to a preserved pyriform sinus. To identify the site, a finger is inserted into the free pyriform sinus through a suprahyoid incision (dotted line). This requires removing the lateral inferior portion of the thyroid cartilage as shown in cross-section.vagus nerves, and, in turn, the function of the stomach. On the other hand, leaving a damaged esophagus in place can result in multiple blind |
Surgery_Schwartz_7231 | Surgery_Schwartz | of the thyroid cartilage as shown in cross-section.vagus nerves, and, in turn, the function of the stomach. On the other hand, leaving a damaged esophagus in place can result in multiple blind sacs and subsequent development of medias-tinal abscesses years later. Most experienced surgeons recom-mend that the esophagus be removed unless the operative risk is unduly high.ACQUIRED FISTULAThe esophagus lies in close contact with the membranous por-tion of the trachea and left bronchus, predisposing to the for-mation of fistula to these structures. Most acquired esophageal fistulas are to the tracheobronchial tree and secondary to either esophageal or pulmonary malignancy. Traumatic fistulas and those associated with esophageal diverticula account for the remainder. Fistulas associated with traction diverticula are usu-ally due to mediastinal inflammatory disease, and traumatic fistulas usually occur secondary to penetrating wounds, lye ingestion, or iatrogenic injury.These fistulas are | Surgery_Schwartz. of the thyroid cartilage as shown in cross-section.vagus nerves, and, in turn, the function of the stomach. On the other hand, leaving a damaged esophagus in place can result in multiple blind sacs and subsequent development of medias-tinal abscesses years later. Most experienced surgeons recom-mend that the esophagus be removed unless the operative risk is unduly high.ACQUIRED FISTULAThe esophagus lies in close contact with the membranous por-tion of the trachea and left bronchus, predisposing to the for-mation of fistula to these structures. Most acquired esophageal fistulas are to the tracheobronchial tree and secondary to either esophageal or pulmonary malignancy. Traumatic fistulas and those associated with esophageal diverticula account for the remainder. Fistulas associated with traction diverticula are usu-ally due to mediastinal inflammatory disease, and traumatic fistulas usually occur secondary to penetrating wounds, lye ingestion, or iatrogenic injury.These fistulas are |
Surgery_Schwartz_7232 | Surgery_Schwartz | traction diverticula are usu-ally due to mediastinal inflammatory disease, and traumatic fistulas usually occur secondary to penetrating wounds, lye ingestion, or iatrogenic injury.These fistulas are characterized by paroxysmal cough-ing following the ingestion of liquids, and by recurrent or chronic pulmonary infections. The onset of cough immediately after swallowing suggests aspiration, whereas a brief delay (30–60 seconds) suggests a fistula.Spontaneous closure is rare, owing to the presence of malignancy or a recurrent infectious process. Surgical treat-ment of benign fistulas consists of division of the fistulous tract, resection of irreversibly damaged lung tissue, and closure of the esophageal defect. To prevent recurrence, a pleural flap should be interposed. Treatment of malignant fistulas is difficult, par-ticularly in the presence of prior irradiation. Generally, only palliative treatment is indicated. This can best be done by using a specially designed esophageal | Surgery_Schwartz. traction diverticula are usu-ally due to mediastinal inflammatory disease, and traumatic fistulas usually occur secondary to penetrating wounds, lye ingestion, or iatrogenic injury.These fistulas are characterized by paroxysmal cough-ing following the ingestion of liquids, and by recurrent or chronic pulmonary infections. The onset of cough immediately after swallowing suggests aspiration, whereas a brief delay (30–60 seconds) suggests a fistula.Spontaneous closure is rare, owing to the presence of malignancy or a recurrent infectious process. Surgical treat-ment of benign fistulas consists of division of the fistulous tract, resection of irreversibly damaged lung tissue, and closure of the esophageal defect. To prevent recurrence, a pleural flap should be interposed. Treatment of malignant fistulas is difficult, par-ticularly in the presence of prior irradiation. Generally, only palliative treatment is indicated. This can best be done by using a specially designed esophageal |
Surgery_Schwartz_7233 | Surgery_Schwartz | malignant fistulas is difficult, par-ticularly in the presence of prior irradiation. Generally, only palliative treatment is indicated. This can best be done by using a specially designed esophageal endoprosthesis that bridges and occludes the fistula, allowing the patient to eat. A salivary tube is also a good option for proximal esophageal fistulas. This tube has a proximal “lip” that rests on the cricopharyngeal muscle and thereby directs the saliva into the tube and past the fis-tula. Rarely, esophageal diversion, coupled with placement of a feeding jejunostomy, can be used as a last resort.Brunicardi_Ch25_p1009-p1098.indd 108801/03/19 6:05 PM 1089ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25of the internal mammary artery and the internal mammary or innominate vein. Removal of the sternoclavicular joint aids in performing the vascular and distal esophageal anastomosis (Fig. 25-83).Reconstruction After Total EsophagectomyNeither the intrathoracic stomach nor the intrathoracic | Surgery_Schwartz. malignant fistulas is difficult, par-ticularly in the presence of prior irradiation. Generally, only palliative treatment is indicated. This can best be done by using a specially designed esophageal endoprosthesis that bridges and occludes the fistula, allowing the patient to eat. A salivary tube is also a good option for proximal esophageal fistulas. This tube has a proximal “lip” that rests on the cricopharyngeal muscle and thereby directs the saliva into the tube and past the fis-tula. Rarely, esophageal diversion, coupled with placement of a feeding jejunostomy, can be used as a last resort.Brunicardi_Ch25_p1009-p1098.indd 108801/03/19 6:05 PM 1089ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25of the internal mammary artery and the internal mammary or innominate vein. Removal of the sternoclavicular joint aids in performing the vascular and distal esophageal anastomosis (Fig. 25-83).Reconstruction After Total EsophagectomyNeither the intrathoracic stomach nor the intrathoracic |
Surgery_Schwartz_7234 | Surgery_Schwartz | sternoclavicular joint aids in performing the vascular and distal esophageal anastomosis (Fig. 25-83).Reconstruction After Total EsophagectomyNeither the intrathoracic stomach nor the intrathoracic colon functions as well as the native esophagus after an esophagogas-trectomy. The choice between these organs will be influenced by several factors, such as the adequacy of their blood supply and the length of resected esophagus that they are capable of bridging. If the stomach shows evidence of disease, or has been contracted or reduced by previous gastric surgery, the length available for esophageal replacement may not be adequate. The presence of diverticular disease, unrecognized carcinoma, or colitis prohibits the use of the colon. The blood supply of the colon is more affected by vascular disease than the blood supply of the stomach, which may prevent its use. Of the two, the colon provides the longest graft. The stomach can usually reach to the neck if the amount of lesser curvature | Surgery_Schwartz. sternoclavicular joint aids in performing the vascular and distal esophageal anastomosis (Fig. 25-83).Reconstruction After Total EsophagectomyNeither the intrathoracic stomach nor the intrathoracic colon functions as well as the native esophagus after an esophagogas-trectomy. The choice between these organs will be influenced by several factors, such as the adequacy of their blood supply and the length of resected esophagus that they are capable of bridging. If the stomach shows evidence of disease, or has been contracted or reduced by previous gastric surgery, the length available for esophageal replacement may not be adequate. The presence of diverticular disease, unrecognized carcinoma, or colitis prohibits the use of the colon. The blood supply of the colon is more affected by vascular disease than the blood supply of the stomach, which may prevent its use. Of the two, the colon provides the longest graft. The stomach can usually reach to the neck if the amount of lesser curvature |
Surgery_Schwartz_7235 | Surgery_Schwartz | disease than the blood supply of the stomach, which may prevent its use. Of the two, the colon provides the longest graft. The stomach can usually reach to the neck if the amount of lesser curvature resected does not interfere with the blood supply to the fundus. Gastric interposition has the advantage that only one anastomosis is required. On the other hand, there is greater potential for aspiration of gastric juice or stricture of the cervical anastomosis from chronic reflux when stomach is used for replacement.Following an esophagogastrectomy, patients may have discomfort during or shortly after eating. The most common symptom is a postprandial pressure sensation or a feeling of being full, which probably results from the loss of the gastric reservoir. This symptom is less common when the colon is used as an esophageal substitute, probably because the distal third of the stomach is retained in the abdomen and the interposed colon provides an additional reservoir function.King and | Surgery_Schwartz. disease than the blood supply of the stomach, which may prevent its use. Of the two, the colon provides the longest graft. The stomach can usually reach to the neck if the amount of lesser curvature resected does not interfere with the blood supply to the fundus. Gastric interposition has the advantage that only one anastomosis is required. On the other hand, there is greater potential for aspiration of gastric juice or stricture of the cervical anastomosis from chronic reflux when stomach is used for replacement.Following an esophagogastrectomy, patients may have discomfort during or shortly after eating. The most common symptom is a postprandial pressure sensation or a feeling of being full, which probably results from the loss of the gastric reservoir. This symptom is less common when the colon is used as an esophageal substitute, probably because the distal third of the stomach is retained in the abdomen and the interposed colon provides an additional reservoir function.King and |
Surgery_Schwartz_7236 | Surgery_Schwartz | the colon is used as an esophageal substitute, probably because the distal third of the stomach is retained in the abdomen and the interposed colon provides an additional reservoir function.King and Hölscher have reported a 40% and 50% inci-dence of dysphagia after reestablishing GI continuity with the stomach following esophagogastrectomy. This incidence is similar to Orringer’s results after using the stomach to replace the esophagus in patients with benign disease. More than one-half of the patients experienced dysphagia postoperatively; TECHNIQUES OF ESOPHAGEAL RECONSTRUCTIONOptions for esophageal substitution include gastric advance-ment, colonic interposition, and either jejunal free transfer or advancement into the chest. Rarely, combinations of these grafts will be the only possible option. The indications for esopha-geal resection and substitution include malignant and end-stage benign disease. The latter includes refluxor drug-induced stricture formation that cannot be | Surgery_Schwartz. the colon is used as an esophageal substitute, probably because the distal third of the stomach is retained in the abdomen and the interposed colon provides an additional reservoir function.King and Hölscher have reported a 40% and 50% inci-dence of dysphagia after reestablishing GI continuity with the stomach following esophagogastrectomy. This incidence is similar to Orringer’s results after using the stomach to replace the esophagus in patients with benign disease. More than one-half of the patients experienced dysphagia postoperatively; TECHNIQUES OF ESOPHAGEAL RECONSTRUCTIONOptions for esophageal substitution include gastric advance-ment, colonic interposition, and either jejunal free transfer or advancement into the chest. Rarely, combinations of these grafts will be the only possible option. The indications for esopha-geal resection and substitution include malignant and end-stage benign disease. The latter includes refluxor drug-induced stricture formation that cannot be |
Surgery_Schwartz_7237 | Surgery_Schwartz | option. The indications for esopha-geal resection and substitution include malignant and end-stage benign disease. The latter includes refluxor drug-induced stricture formation that cannot be dilated without damage to the esophagus, a dilated and tortuous esophagus secondary to severe motility disorders, lye-induced strictures, and multiple previous antireflux procedures. The choice of esophageal substitution has significant impact upon the technical difficulty of the procedure and influences the long-term outcome.Partial Esophageal ResectionDistal benign lesions, with preserved proximal esophageal func-tion, are best treated with the interposition of a segment of prox-imal jejunum into the chest and primary anastomosis. A jejunal interposition can reach to the inferior border of the pulmonary hilum with ease, but the architecture of its blood supply rarely allows the use of the jejunum proximal to this point. Because the anastomosis is within the chest, a thoracotomy is necessary.The | Surgery_Schwartz. option. The indications for esopha-geal resection and substitution include malignant and end-stage benign disease. The latter includes refluxor drug-induced stricture formation that cannot be dilated without damage to the esophagus, a dilated and tortuous esophagus secondary to severe motility disorders, lye-induced strictures, and multiple previous antireflux procedures. The choice of esophageal substitution has significant impact upon the technical difficulty of the procedure and influences the long-term outcome.Partial Esophageal ResectionDistal benign lesions, with preserved proximal esophageal func-tion, are best treated with the interposition of a segment of prox-imal jejunum into the chest and primary anastomosis. A jejunal interposition can reach to the inferior border of the pulmonary hilum with ease, but the architecture of its blood supply rarely allows the use of the jejunum proximal to this point. Because the anastomosis is within the chest, a thoracotomy is necessary.The |
Surgery_Schwartz_7238 | Surgery_Schwartz | hilum with ease, but the architecture of its blood supply rarely allows the use of the jejunum proximal to this point. Because the anastomosis is within the chest, a thoracotomy is necessary.The jejunum is a dynamic graft and contributes to bolus transport, whereas the stomach and colon function more as a conduit. The stomach is a poor choice in this circumstance because of the propensity for the reflux of gastric contents into the proximal remaining esophagus following an intratho-racic esophagogastrostomy. It is now well recognized that this occurs and can lead to incapacitating symptoms and esophageal destruction in some patients. Short segments of colon, on the other hand, lack significant motility and have a propensity for the development of esophagitis proximal to the anastomosis.Replacement of the cervical portion of the esophagus, while preserving the distal portion, is occasionally indicated in cervical esophageal or head and neck malignancy, and follow-ing the ingestion of | Surgery_Schwartz. hilum with ease, but the architecture of its blood supply rarely allows the use of the jejunum proximal to this point. Because the anastomosis is within the chest, a thoracotomy is necessary.The jejunum is a dynamic graft and contributes to bolus transport, whereas the stomach and colon function more as a conduit. The stomach is a poor choice in this circumstance because of the propensity for the reflux of gastric contents into the proximal remaining esophagus following an intratho-racic esophagogastrostomy. It is now well recognized that this occurs and can lead to incapacitating symptoms and esophageal destruction in some patients. Short segments of colon, on the other hand, lack significant motility and have a propensity for the development of esophagitis proximal to the anastomosis.Replacement of the cervical portion of the esophagus, while preserving the distal portion, is occasionally indicated in cervical esophageal or head and neck malignancy, and follow-ing the ingestion of |
Surgery_Schwartz_7239 | Surgery_Schwartz | of the cervical portion of the esophagus, while preserving the distal portion, is occasionally indicated in cervical esophageal or head and neck malignancy, and follow-ing the ingestion of lye. Free transfer of a portion of jejunum to the neck has become a viable option and is successful in the majority of cases. Revascularization is achieved via use Figure 25-83. A. The portion of the thoracic inlet to be resected to provide space for a free jejunal graft and access to the internal mammary artery (shaded area). B. Cross-section showing the space available after resection of the sternoclavicular joint and one-half of the manubrium. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Brunicardi_Ch25_p1009-p1098.indd 108901/03/19 6:06 PM 1090SPECIFIC CONSIDERATIONSPART IItwo-thirds of this group required postoperative dilation, and one-fourth had persistent dysphagia and required home dilation. In contrast, dysphagia | Surgery_Schwartz. of the cervical portion of the esophagus, while preserving the distal portion, is occasionally indicated in cervical esophageal or head and neck malignancy, and follow-ing the ingestion of lye. Free transfer of a portion of jejunum to the neck has become a viable option and is successful in the majority of cases. Revascularization is achieved via use Figure 25-83. A. The portion of the thoracic inlet to be resected to provide space for a free jejunal graft and access to the internal mammary artery (shaded area). B. Cross-section showing the space available after resection of the sternoclavicular joint and one-half of the manubrium. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Brunicardi_Ch25_p1009-p1098.indd 108901/03/19 6:06 PM 1090SPECIFIC CONSIDERATIONSPART IItwo-thirds of this group required postoperative dilation, and one-fourth had persistent dysphagia and required home dilation. In contrast, dysphagia |
Surgery_Schwartz_7240 | Surgery_Schwartz | 6:06 PM 1090SPECIFIC CONSIDERATIONSPART IItwo-thirds of this group required postoperative dilation, and one-fourth had persistent dysphagia and required home dilation. In contrast, dysphagia is uncommon, and the need for dilation is rare following a colonic interposition. Isolauri reported on 248 patients with colonic interpositions and noted a 24% incidence of dysphagia 12 months after the operation. When it occurred, the most common cause was recurrent mediastinal tumor. The high incidence of dysphagia with the use of the stomach is prob-ably related to the esophagogastric anastomosis in the neck and the resulting difficulty of passing a swallowed bolus.Another consequence of the transposition of the stomach into the chest is the development of postoperative duodenogastric reflux, probably due to pyloric denervation, and adding a pyloroplasty may worsen this problem. Following gastric advancement, the pylorus lies at the level of the esophageal hiatus, and a distinct pressure | Surgery_Schwartz. 6:06 PM 1090SPECIFIC CONSIDERATIONSPART IItwo-thirds of this group required postoperative dilation, and one-fourth had persistent dysphagia and required home dilation. In contrast, dysphagia is uncommon, and the need for dilation is rare following a colonic interposition. Isolauri reported on 248 patients with colonic interpositions and noted a 24% incidence of dysphagia 12 months after the operation. When it occurred, the most common cause was recurrent mediastinal tumor. The high incidence of dysphagia with the use of the stomach is prob-ably related to the esophagogastric anastomosis in the neck and the resulting difficulty of passing a swallowed bolus.Another consequence of the transposition of the stomach into the chest is the development of postoperative duodenogastric reflux, probably due to pyloric denervation, and adding a pyloroplasty may worsen this problem. Following gastric advancement, the pylorus lies at the level of the esophageal hiatus, and a distinct pressure |
Surgery_Schwartz_7241 | Surgery_Schwartz | probably due to pyloric denervation, and adding a pyloroplasty may worsen this problem. Following gastric advancement, the pylorus lies at the level of the esophageal hiatus, and a distinct pressure differential develops between the intrathoracic gastric and intra-abdominal duodenal lumina. Unless the pyloric valve is extremely efficient, the pressure differential will encourage reflux of duodenal contents into the stomach. Duodenogastric reflux is less likely to occur following colonic interposition because there is sufficient intra-abdominal colon to be compressed by the abdominal pressure and the pylorus and duodenum remain in their normal intra-abdominal position.Although there is general acceptance of the concept that an esophagogastric anastomosis in the neck results in less post-operative esophagitis and stricture than one at a lower level, reflux esophagitis following a cervical anastomosis does occur, albeit at a lower rate than when the anastomosis is at a lower level. Most | Surgery_Schwartz. probably due to pyloric denervation, and adding a pyloroplasty may worsen this problem. Following gastric advancement, the pylorus lies at the level of the esophageal hiatus, and a distinct pressure differential develops between the intrathoracic gastric and intra-abdominal duodenal lumina. Unless the pyloric valve is extremely efficient, the pressure differential will encourage reflux of duodenal contents into the stomach. Duodenogastric reflux is less likely to occur following colonic interposition because there is sufficient intra-abdominal colon to be compressed by the abdominal pressure and the pylorus and duodenum remain in their normal intra-abdominal position.Although there is general acceptance of the concept that an esophagogastric anastomosis in the neck results in less post-operative esophagitis and stricture than one at a lower level, reflux esophagitis following a cervical anastomosis does occur, albeit at a lower rate than when the anastomosis is at a lower level. Most |
Surgery_Schwartz_7242 | Surgery_Schwartz | esophagitis and stricture than one at a lower level, reflux esophagitis following a cervical anastomosis does occur, albeit at a lower rate than when the anastomosis is at a lower level. Most patients undergo cervical esophagogastrostomy for malignancy; thus, the long-term sequelae of an esophagogastric anastomosis in the neck are not of concern. However, patients who have had a cervical esophagogastrostomy for benign dis-ease may develop problems associated with the anastomosis in the fourth or fifth postoperative year that are severe enough to require anastomotic revision. This is less likely in patients who have had a colonic interposition for esophageal replace-ment. Consequently, in patients who have a benign process or a potentially curable carcinoma of the esophagus or cardia, a colonic interposition is used to obviate the late problems associ-ated with a cervical esophagogastrostomy. Colonic interposition for esophageal substitution is a more complex procedure than gastric | Surgery_Schwartz. esophagitis and stricture than one at a lower level, reflux esophagitis following a cervical anastomosis does occur, albeit at a lower rate than when the anastomosis is at a lower level. Most patients undergo cervical esophagogastrostomy for malignancy; thus, the long-term sequelae of an esophagogastric anastomosis in the neck are not of concern. However, patients who have had a cervical esophagogastrostomy for benign dis-ease may develop problems associated with the anastomosis in the fourth or fifth postoperative year that are severe enough to require anastomotic revision. This is less likely in patients who have had a colonic interposition for esophageal replace-ment. Consequently, in patients who have a benign process or a potentially curable carcinoma of the esophagus or cardia, a colonic interposition is used to obviate the late problems associ-ated with a cervical esophagogastrostomy. Colonic interposition for esophageal substitution is a more complex procedure than gastric |
Surgery_Schwartz_7243 | Surgery_Schwartz | colonic interposition is used to obviate the late problems associ-ated with a cervical esophagogastrostomy. Colonic interposition for esophageal substitution is a more complex procedure than gastric advancement, with the potential for greater perioperative morbidity, particularly in inexperienced hands.Composite ReconstructionOccasionally, a combination of colon, jejunum, and stomach is the only reconstructive option available. This situation may arise when there has been previous gastric or colonic resection, when dysphagia has recurred after a previous esophageal resec-tion, or following postoperative complications such as ischemia of an esophageal substitute. Although not ideal, combinations of colon, jejunum, and stomach used to restore GI continuity function surprisingly well and allow alimentary reconstruction in an otherwise impossible situation.Vagal Sparing Esophagectomy With Colon InterpositionTraditional esophagectomy typically results in bilateral vagot-omy and its | Surgery_Schwartz. colonic interposition is used to obviate the late problems associ-ated with a cervical esophagogastrostomy. Colonic interposition for esophageal substitution is a more complex procedure than gastric advancement, with the potential for greater perioperative morbidity, particularly in inexperienced hands.Composite ReconstructionOccasionally, a combination of colon, jejunum, and stomach is the only reconstructive option available. This situation may arise when there has been previous gastric or colonic resection, when dysphagia has recurred after a previous esophageal resec-tion, or following postoperative complications such as ischemia of an esophageal substitute. Although not ideal, combinations of colon, jejunum, and stomach used to restore GI continuity function surprisingly well and allow alimentary reconstruction in an otherwise impossible situation.Vagal Sparing Esophagectomy With Colon InterpositionTraditional esophagectomy typically results in bilateral vagot-omy and its |
Surgery_Schwartz_7244 | Surgery_Schwartz | and allow alimentary reconstruction in an otherwise impossible situation.Vagal Sparing Esophagectomy With Colon InterpositionTraditional esophagectomy typically results in bilateral vagot-omy and its attendant consequences. It is likely that symptoms such as dumping, diarrhea, early satiety, and weight loss seen in 15% to 20% of patients postesophagectomy are at least in part, if not completely, due to vagal interruption. The technique of vagal sparing esophagectomy with colon interposition has been described in an effort to avoid the morbidities associated with standard esophagectomy.Through an upper midline abdominal incision, the right and left vagal nerves are identified, circled with a tape, and retracted to the right. A limited, highly selective proximal gas-tric vagotomy is performed along the cephalad 4 cm of the lesser curvature. The stomach is divided with an Endo-GIA stapler just below the GEJ. The colon is prepared to provide an interposed segment as previously described. | Surgery_Schwartz. and allow alimentary reconstruction in an otherwise impossible situation.Vagal Sparing Esophagectomy With Colon InterpositionTraditional esophagectomy typically results in bilateral vagot-omy and its attendant consequences. It is likely that symptoms such as dumping, diarrhea, early satiety, and weight loss seen in 15% to 20% of patients postesophagectomy are at least in part, if not completely, due to vagal interruption. The technique of vagal sparing esophagectomy with colon interposition has been described in an effort to avoid the morbidities associated with standard esophagectomy.Through an upper midline abdominal incision, the right and left vagal nerves are identified, circled with a tape, and retracted to the right. A limited, highly selective proximal gas-tric vagotomy is performed along the cephalad 4 cm of the lesser curvature. The stomach is divided with an Endo-GIA stapler just below the GEJ. The colon is prepared to provide an interposed segment as previously described. |
Surgery_Schwartz_7245 | Surgery_Schwartz | along the cephalad 4 cm of the lesser curvature. The stomach is divided with an Endo-GIA stapler just below the GEJ. The colon is prepared to provide an interposed segment as previously described. A neck incision is made along the anterior border of the left sternocleidomastoid muscle, and the strap muscles are exposed. The omohyoid muscle is divided at its pulley, and the sternohyoid and sternothyroid muscles are divided at their manubrial insertion. The left carotid sheath is retracted laterally and the thyroid and trachea medially. The left inferior thyroid artery is ligated laterally as it passes under the left common carotid artery. The left recurrent laryngeal nerve is identified and protected. The esophagus is dissected circumfer-entially in an inferior direction, from the left neck to the apex of the right chest, to avoid injury to the right recurrent laryngeal nerve. The esophagus is divided at the level of the thoracic inlet, leaving about 3 to 4 cm of cervical esophagus. | Surgery_Schwartz. along the cephalad 4 cm of the lesser curvature. The stomach is divided with an Endo-GIA stapler just below the GEJ. The colon is prepared to provide an interposed segment as previously described. A neck incision is made along the anterior border of the left sternocleidomastoid muscle, and the strap muscles are exposed. The omohyoid muscle is divided at its pulley, and the sternohyoid and sternothyroid muscles are divided at their manubrial insertion. The left carotid sheath is retracted laterally and the thyroid and trachea medially. The left inferior thyroid artery is ligated laterally as it passes under the left common carotid artery. The left recurrent laryngeal nerve is identified and protected. The esophagus is dissected circumfer-entially in an inferior direction, from the left neck to the apex of the right chest, to avoid injury to the right recurrent laryngeal nerve. The esophagus is divided at the level of the thoracic inlet, leaving about 3 to 4 cm of cervical esophagus. |
Surgery_Schwartz_7246 | Surgery_Schwartz | to the apex of the right chest, to avoid injury to the right recurrent laryngeal nerve. The esophagus is divided at the level of the thoracic inlet, leaving about 3 to 4 cm of cervical esophagus. The proximal esophagus is retracted anteriorly and to the right with the use of two sutures to keep saliva and oral contents from contaminating the neck wound.Returning to the abdomen, the proximal staple line of the gastric division is opened, and the esophagus is flushed with povidone-iodine solution. A vein stripper is passed up the esophagus into the neck wound. The distal portion of the esophagus in the neck is secured tightly around the stripping cable with “endoloops” and an umbilical tape for a trailer. The tip of the stripper is exchanged for a mushroom head, and the stripper is pulled back into the abdomen, inverting the esopha-gus as it transverses the posterior mediastinum. This maneuver strips the branches of the esophageal plexus off the longitudi-nal muscle of the esophagus, | Surgery_Schwartz. to the apex of the right chest, to avoid injury to the right recurrent laryngeal nerve. The esophagus is divided at the level of the thoracic inlet, leaving about 3 to 4 cm of cervical esophagus. The proximal esophagus is retracted anteriorly and to the right with the use of two sutures to keep saliva and oral contents from contaminating the neck wound.Returning to the abdomen, the proximal staple line of the gastric division is opened, and the esophagus is flushed with povidone-iodine solution. A vein stripper is passed up the esophagus into the neck wound. The distal portion of the esophagus in the neck is secured tightly around the stripping cable with “endoloops” and an umbilical tape for a trailer. The tip of the stripper is exchanged for a mushroom head, and the stripper is pulled back into the abdomen, inverting the esopha-gus as it transverses the posterior mediastinum. This maneuver strips the branches of the esophageal plexus off the longitudi-nal muscle of the esophagus, |
Surgery_Schwartz_7247 | Surgery_Schwartz | back into the abdomen, inverting the esopha-gus as it transverses the posterior mediastinum. This maneuver strips the branches of the esophageal plexus off the longitudi-nal muscle of the esophagus, preserving the esophageal plexus along with the proximal vagal nerves and the distal vagal nerve trunks. In patients with end-stage achalasia, only the mucosa is secured around the stripping cable, so that it alone is stripped and the dilated muscular wall of the esophagus, with its enriched blood supply, remains. The resulting medi-astinal tunnel, or in the case of achalasia the muscular tube, is dilated with a Foley catheter containing 90 mL of fluid in the balloon. The previously prepared interposed portion of the transverse colon is passed behind the stomach and up through the mediastinal tunnel into the neck. An end-to-end anastomo-sis is performed to the cervical esophagus using a single layer technique. The colon is pulled taut and secured to the left crus with four or five | Surgery_Schwartz. back into the abdomen, inverting the esopha-gus as it transverses the posterior mediastinum. This maneuver strips the branches of the esophageal plexus off the longitudi-nal muscle of the esophagus, preserving the esophageal plexus along with the proximal vagal nerves and the distal vagal nerve trunks. In patients with end-stage achalasia, only the mucosa is secured around the stripping cable, so that it alone is stripped and the dilated muscular wall of the esophagus, with its enriched blood supply, remains. The resulting medi-astinal tunnel, or in the case of achalasia the muscular tube, is dilated with a Foley catheter containing 90 mL of fluid in the balloon. The previously prepared interposed portion of the transverse colon is passed behind the stomach and up through the mediastinal tunnel into the neck. An end-to-end anastomo-sis is performed to the cervical esophagus using a single layer technique. The colon is pulled taut and secured to the left crus with four or five |
Surgery_Schwartz_7248 | Surgery_Schwartz | tunnel into the neck. An end-to-end anastomo-sis is performed to the cervical esophagus using a single layer technique. The colon is pulled taut and secured to the left crus with four or five interrupted sutures. Five centimeters below the crura an opening is made in the mesentery adjacent to the colon along its mesenteric border, through which an Endo-GIA stapler is passed and the colon is divided. The proximal end, which is the distal end of the interposed colon, is anasto-mosed high on the posterior fundic wall of the stomach, using a triangular stapling anastomotic technique. This is done by stapling longitudinally the stomach and colon together with a 75-mm Endo-GIA stapler, spreading the base of the incision apart, and closing it with a T-55 stapler. Colonic continuity is reestablished by bringing the proximal right colon to the dis-tal staple line in the left colon and performing an end-to-end anastomosis using a double-layer technique.Brunicardi_Ch25_p1009-p1098.indd | Surgery_Schwartz. tunnel into the neck. An end-to-end anastomo-sis is performed to the cervical esophagus using a single layer technique. The colon is pulled taut and secured to the left crus with four or five interrupted sutures. Five centimeters below the crura an opening is made in the mesentery adjacent to the colon along its mesenteric border, through which an Endo-GIA stapler is passed and the colon is divided. The proximal end, which is the distal end of the interposed colon, is anasto-mosed high on the posterior fundic wall of the stomach, using a triangular stapling anastomotic technique. This is done by stapling longitudinally the stomach and colon together with a 75-mm Endo-GIA stapler, spreading the base of the incision apart, and closing it with a T-55 stapler. Colonic continuity is reestablished by bringing the proximal right colon to the dis-tal staple line in the left colon and performing an end-to-end anastomosis using a double-layer technique.Brunicardi_Ch25_p1009-p1098.indd |
Surgery_Schwartz_7249 | Surgery_Schwartz | by bringing the proximal right colon to the dis-tal staple line in the left colon and performing an end-to-end anastomosis using a double-layer technique.Brunicardi_Ch25_p1009-p1098.indd 109001/03/19 6:06 PM 1091ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Although conceptually appealing, preservation of vagal nerve integrity or the gastric reservoir function after vagal spar-ing esophagectomy only recently has been validated. Banki and associates compared patients undergoing vagal sparing esopha-gectomy to those with conventional esophagectomy and colon or gastric interposition. This study showed that vagal sparing esophagectomy preserved gastric secretion, gastric emptying, meal capacity, and body mass index, compared to esophagogas-trectomy with colon interposition or standard esophagectomy with gastric pull-up. Vagal sparing esophagectomy patients functioned, for the most part, similarly to normal subjects, allowing them to eat a normal meal, free of dumping or diarrhea. These | Surgery_Schwartz. by bringing the proximal right colon to the dis-tal staple line in the left colon and performing an end-to-end anastomosis using a double-layer technique.Brunicardi_Ch25_p1009-p1098.indd 109001/03/19 6:06 PM 1091ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Although conceptually appealing, preservation of vagal nerve integrity or the gastric reservoir function after vagal spar-ing esophagectomy only recently has been validated. Banki and associates compared patients undergoing vagal sparing esopha-gectomy to those with conventional esophagectomy and colon or gastric interposition. This study showed that vagal sparing esophagectomy preserved gastric secretion, gastric emptying, meal capacity, and body mass index, compared to esophagogas-trectomy with colon interposition or standard esophagectomy with gastric pull-up. Vagal sparing esophagectomy patients functioned, for the most part, similarly to normal subjects, allowing them to eat a normal meal, free of dumping or diarrhea. These |
Surgery_Schwartz_7250 | Surgery_Schwartz | with gastric pull-up. Vagal sparing esophagectomy patients functioned, for the most part, similarly to normal subjects, allowing them to eat a normal meal, free of dumping or diarrhea. These results indicate that the vagal-sparing esophagectomy procedure does indeed preserve the vagal nerves, and it may be considered in the treatment of benign and early malignant lesions requiring esophagectomy.BIBLIOGRAPHYEntries highlighted in bright blue are key references.General ReferencesBalaji B, Peters JH. Minimally invasive surgery for esophageal motor disorders. Surg Clin North Am. 2002;82:763-782.Bremner CG, DeMeester TR, Bremner RM. Esophageal Motility Testing Made Easy. St. Louis: Quality Medical Publishing, 2001.Castel DW, Richter J, eds. The Esophagus. Boston: Little, Brown & Co., 1999.DeMeester SR, Peters JH, DeMeester TR. Barrett’s esophagus. Curr Probl Surg. 2001;38:549-640.Demeester SR, ed. Barrett’s esophagus. Problems in General Surgery. Vol. 18, no. 2. Hagerstown, MD: | Surgery_Schwartz. with gastric pull-up. Vagal sparing esophagectomy patients functioned, for the most part, similarly to normal subjects, allowing them to eat a normal meal, free of dumping or diarrhea. These results indicate that the vagal-sparing esophagectomy procedure does indeed preserve the vagal nerves, and it may be considered in the treatment of benign and early malignant lesions requiring esophagectomy.BIBLIOGRAPHYEntries highlighted in bright blue are key references.General ReferencesBalaji B, Peters JH. Minimally invasive surgery for esophageal motor disorders. Surg Clin North Am. 2002;82:763-782.Bremner CG, DeMeester TR, Bremner RM. Esophageal Motility Testing Made Easy. St. Louis: Quality Medical Publishing, 2001.Castel DW, Richter J, eds. The Esophagus. Boston: Little, Brown & Co., 1999.DeMeester SR, Peters JH, DeMeester TR. Barrett’s esophagus. Curr Probl Surg. 2001;38:549-640.Demeester SR, ed. Barrett’s esophagus. Problems in General Surgery. Vol. 18, no. 2. Hagerstown, MD: |
Surgery_Schwartz_7251 | Surgery_Schwartz | 1999.DeMeester SR, Peters JH, DeMeester TR. Barrett’s esophagus. Curr Probl Surg. 2001;38:549-640.Demeester SR, ed. Barrett’s esophagus. Problems in General Surgery. Vol. 18, no. 2. Hagerstown, MD: Lippincott Williams & Wilkins; 2001.DeMeester TR, Peters JH, Bremner CG, et al. Biology of gastro-esophageal reflux disease; pathophysiology relating to medical and surgical treatment. Annu Rev Med. 1999;50:469-506.Hunter JG, Pellagrini CA. Surgery of the esophagus. Surg Clin North Am. 1997;77:959-970.McFadyen BV, Arregui ME, Eubanks S, et al. Laparoscopic Surgery of the Abdomen. New York: Springer, 2003.Surgical AnatomyDaffner RH, Halber MD, Postlethwait RW, et al. CT of the esopha-gus. II. Carcinoma. AJR Am J Roentgenol. 1979;133:1051-1055.Gray SW, Rowe JS Jr, Skandalakis JE. Surgical anatomy of the gastroesophageal junction. Am Surg. 1979;45:575-587.Liebermann-Meffert D. The pharyngoesophageal segment: anat-omy and innervation. Dis Esophagus. 1995;8:242-251.Liebermann-Meffert D, | Surgery_Schwartz. 1999.DeMeester SR, Peters JH, DeMeester TR. Barrett’s esophagus. Curr Probl Surg. 2001;38:549-640.Demeester SR, ed. Barrett’s esophagus. Problems in General Surgery. Vol. 18, no. 2. Hagerstown, MD: Lippincott Williams & Wilkins; 2001.DeMeester TR, Peters JH, Bremner CG, et al. Biology of gastro-esophageal reflux disease; pathophysiology relating to medical and surgical treatment. Annu Rev Med. 1999;50:469-506.Hunter JG, Pellagrini CA. Surgery of the esophagus. Surg Clin North Am. 1997;77:959-970.McFadyen BV, Arregui ME, Eubanks S, et al. Laparoscopic Surgery of the Abdomen. New York: Springer, 2003.Surgical AnatomyDaffner RH, Halber MD, Postlethwait RW, et al. CT of the esopha-gus. II. Carcinoma. AJR Am J Roentgenol. 1979;133:1051-1055.Gray SW, Rowe JS Jr, Skandalakis JE. Surgical anatomy of the gastroesophageal junction. Am Surg. 1979;45:575-587.Liebermann-Meffert D. The pharyngoesophageal segment: anat-omy and innervation. Dis Esophagus. 1995;8:242-251.Liebermann-Meffert D, |
Surgery_Schwartz_7252 | Surgery_Schwartz | anatomy of the gastroesophageal junction. Am Surg. 1979;45:575-587.Liebermann-Meffert D. The pharyngoesophageal segment: anat-omy and innervation. Dis Esophagus. 1995;8:242-251.Liebermann-Meffert D, Siewert JR. Arterial anatomy of the esopha-gus: a review of the literature with brief comments on clinical aspects. Gullet. 1992;2:3-10.Liebermann-Meffert DM, Meier R, Siewert JR. Vascular anat-omy of the gastric tube used for esophageal reconstruction. Ann Thorac Surg. 1992;54(6):1110-1115.Liebermann-Meffert DM, Walbrun B, Hiebert CA, et al. Recurrent and superior laryngeal nerves: a new look with implications for the esophageal surgeon. Ann Thorac Surg. 1999;67:217-223.PhysiologyBarlow AP, DeMeester TR, Ball CS, et al. The significance of the gastric secretory state in gastroesophageal reflux disease. Arch Surg. 1989;124:937-940.DeMeester TR, Lafontaine E, Joelsson BE, et al. The relation-ship of a hiatal hernia to the function of the body of the esophagus and the gastroesophageal | Surgery_Schwartz. anatomy of the gastroesophageal junction. Am Surg. 1979;45:575-587.Liebermann-Meffert D. The pharyngoesophageal segment: anat-omy and innervation. Dis Esophagus. 1995;8:242-251.Liebermann-Meffert D, Siewert JR. Arterial anatomy of the esopha-gus: a review of the literature with brief comments on clinical aspects. Gullet. 1992;2:3-10.Liebermann-Meffert DM, Meier R, Siewert JR. Vascular anat-omy of the gastric tube used for esophageal reconstruction. Ann Thorac Surg. 1992;54(6):1110-1115.Liebermann-Meffert DM, Walbrun B, Hiebert CA, et al. Recurrent and superior laryngeal nerves: a new look with implications for the esophageal surgeon. Ann Thorac Surg. 1999;67:217-223.PhysiologyBarlow AP, DeMeester TR, Ball CS, et al. The significance of the gastric secretory state in gastroesophageal reflux disease. Arch Surg. 1989;124:937-940.DeMeester TR, Lafontaine E, Joelsson BE, et al. The relation-ship of a hiatal hernia to the function of the body of the esophagus and the gastroesophageal |
Surgery_Schwartz_7253 | Surgery_Schwartz | reflux disease. Arch Surg. 1989;124:937-940.DeMeester TR, Lafontaine E, Joelsson BE, et al. The relation-ship of a hiatal hernia to the function of the body of the esophagus and the gastroesophageal junction. J Thorac Car-diovasc Surg. 1981;82(4):547-558.Helm JF, Dodds WJ, Pelc LR, Palmer DW, Hogan WJ, Teeter BC. Effect of esophageal emptying and saliva on clearance of acid from the esophagus. N Engl J Med. 1984;310:284-288.Joelsson BE, DeMeester TR, Skinner DB, LaFontaine E, Waters PF, O’Sullivan GC. The role of the esophageal body in the antire-flux mechanism. Surgery. 1982;92:417-424.Johnson LF, DeMeester TR. Evaluation of elevation of the head of the bed, bethanechol, and antacid foam tablets on gastroesopha-geal reflux. Dig Dis Sci. 1981;26:673-680.Kahrilas PJ, Dodds WJ, Hogan WJ. Effect of peristaltic dysfunc-tion on esophageal volume clearance. Gastroenterology. 1988;94:73-80.McCallum RW, Berkowitz DM, Lerner E. Gastric emptying in patients with gastroesophageal reflux. | Surgery_Schwartz. reflux disease. Arch Surg. 1989;124:937-940.DeMeester TR, Lafontaine E, Joelsson BE, et al. The relation-ship of a hiatal hernia to the function of the body of the esophagus and the gastroesophageal junction. J Thorac Car-diovasc Surg. 1981;82(4):547-558.Helm JF, Dodds WJ, Pelc LR, Palmer DW, Hogan WJ, Teeter BC. Effect of esophageal emptying and saliva on clearance of acid from the esophagus. N Engl J Med. 1984;310:284-288.Joelsson BE, DeMeester TR, Skinner DB, LaFontaine E, Waters PF, O’Sullivan GC. The role of the esophageal body in the antire-flux mechanism. Surgery. 1982;92:417-424.Johnson LF, DeMeester TR. Evaluation of elevation of the head of the bed, bethanechol, and antacid foam tablets on gastroesopha-geal reflux. Dig Dis Sci. 1981;26:673-680.Kahrilas PJ, Dodds WJ, Hogan WJ. Effect of peristaltic dysfunc-tion on esophageal volume clearance. Gastroenterology. 1988;94:73-80.McCallum RW, Berkowitz DM, Lerner E. Gastric emptying in patients with gastroesophageal reflux. |
Surgery_Schwartz_7254 | Surgery_Schwartz | WJ. Effect of peristaltic dysfunc-tion on esophageal volume clearance. Gastroenterology. 1988;94:73-80.McCallum RW, Berkowitz DM, Lerner E. Gastric emptying in patients with gastroesophageal reflux. Gastroenterology. 1981;80:285-291.Mittal RK, Lange RC, McCallum RW. Identification and mecha-nism of delayed esophageal acid clearance in subjects with hiatus hernia. Gastroenterology. 1987;92:130-135.Rao SSC, Madipalli RS, Mujica VR, et al. Effects of age and gender on esophageal biomechanical properties and sensation. Am J Gastroenterol. 2003;98:1688-1695.Tseng D, Rizvi AZ, Fennerty MB, et al. Forty-eight-hour pH moni-toring increases sensitivity in detecting abnormal esophageal acid exposure. J Gastrointest Surg. 2005;9:1043-1051; discussion 1051.Zaninotto G, DeMeester TR, Schwizer W, et al. The lower esophageal sphincter in health and disease. Am J Surg. 1988;155:104-111.Assessment of Esophageal FunctionAdamek RJ, Wegener M, Weinbeck M, Gielen B. Long-term esoph-ageal manometry in | Surgery_Schwartz. WJ. Effect of peristaltic dysfunc-tion on esophageal volume clearance. Gastroenterology. 1988;94:73-80.McCallum RW, Berkowitz DM, Lerner E. Gastric emptying in patients with gastroesophageal reflux. Gastroenterology. 1981;80:285-291.Mittal RK, Lange RC, McCallum RW. Identification and mecha-nism of delayed esophageal acid clearance in subjects with hiatus hernia. Gastroenterology. 1987;92:130-135.Rao SSC, Madipalli RS, Mujica VR, et al. Effects of age and gender on esophageal biomechanical properties and sensation. Am J Gastroenterol. 2003;98:1688-1695.Tseng D, Rizvi AZ, Fennerty MB, et al. Forty-eight-hour pH moni-toring increases sensitivity in detecting abnormal esophageal acid exposure. J Gastrointest Surg. 2005;9:1043-1051; discussion 1051.Zaninotto G, DeMeester TR, Schwizer W, et al. The lower esophageal sphincter in health and disease. Am J Surg. 1988;155:104-111.Assessment of Esophageal FunctionAdamek RJ, Wegener M, Weinbeck M, Gielen B. Long-term esoph-ageal manometry in |
Surgery_Schwartz_7255 | Surgery_Schwartz | al. The lower esophageal sphincter in health and disease. Am J Surg. 1988;155:104-111.Assessment of Esophageal FunctionAdamek RJ, Wegener M, Weinbeck M, Gielen B. Long-term esoph-ageal manometry in healthy subjects: evaluation of normal values and influence of age. Dig Dis Sci. 1994;39:2069-2073.Barish CF, Castell DO, Richter JE. Graded esophageal balloon distention: a new provocative test for non-cardiac chest pain. Dig Dis Sci. 1986;31:1292-1298.Battle WS, Nyhus LM, Bombeck CT. Gastroesophageal reflux: diagnosis and treatment. Ann Surg. 1973;177:560-565.Bernstein IM, Baker CA. A clinical test for esophagitis. Gastroen-terology. 1958;34:760-781.DeMeester TR, Johnson LF, Joseph GJ, Toscano MS, Hall AW, Skinner DB. Patterns of gastroesophageal reflux in health and disease. Ann Surg. 1976;184(4):459-470.DeMeester TR, Wang CI, Wernly JA, et al. Technique, indications and clinical use of 24-hour esophageal pH monitoring. J Thorac Cardiovasc Surg. 1980;79:656-670.Dodds WJ. Current | Surgery_Schwartz. al. The lower esophageal sphincter in health and disease. Am J Surg. 1988;155:104-111.Assessment of Esophageal FunctionAdamek RJ, Wegener M, Weinbeck M, Gielen B. Long-term esoph-ageal manometry in healthy subjects: evaluation of normal values and influence of age. Dig Dis Sci. 1994;39:2069-2073.Barish CF, Castell DO, Richter JE. Graded esophageal balloon distention: a new provocative test for non-cardiac chest pain. Dig Dis Sci. 1986;31:1292-1298.Battle WS, Nyhus LM, Bombeck CT. Gastroesophageal reflux: diagnosis and treatment. Ann Surg. 1973;177:560-565.Bernstein IM, Baker CA. A clinical test for esophagitis. Gastroen-terology. 1958;34:760-781.DeMeester TR, Johnson LF, Joseph GJ, Toscano MS, Hall AW, Skinner DB. Patterns of gastroesophageal reflux in health and disease. Ann Surg. 1976;184(4):459-470.DeMeester TR, Wang CI, Wernly JA, et al. Technique, indications and clinical use of 24-hour esophageal pH monitoring. J Thorac Cardiovasc Surg. 1980;79:656-670.Dodds WJ. Current |
Surgery_Schwartz_7256 | Surgery_Schwartz | 1976;184(4):459-470.DeMeester TR, Wang CI, Wernly JA, et al. Technique, indications and clinical use of 24-hour esophageal pH monitoring. J Thorac Cardiovasc Surg. 1980;79:656-670.Dodds WJ. Current concepts of esophageal motor function: clinical implications for radiology. AJR Am J Roentgenol. 1977;128:549-561.Fein M, Fuchs KH, Bohrer T, et al. Fiberoptic technique for 24-hour bile reflux monitoring. Standards and normal values for gastric monitoring. Dig Dis Sci. 1996;41:216-225.Fuchs KH, DeMeester TR, Albertucci M. Specificity and sensitiv-ity of objective diagnosis of gastroesophageal reflux disease. Surgery. 1987;102:575-580.Iascone C, DeMeester TR, et al. Barrett’s esophagus: functional assessment, proposed pathogenesis, and surgical therapy. Arch Surg. 1983;118:543-549.Johnson LF, DeMeester TR. Development of 24-hour intra-esophageal pH monitoring composite scoring. J Clin Gastroenterol. 1986;8(suppl 1):52-58.Johnson LF, DeMeester TR. Twenty-four-hour pH monitoring of the | Surgery_Schwartz. 1976;184(4):459-470.DeMeester TR, Wang CI, Wernly JA, et al. Technique, indications and clinical use of 24-hour esophageal pH monitoring. J Thorac Cardiovasc Surg. 1980;79:656-670.Dodds WJ. Current concepts of esophageal motor function: clinical implications for radiology. AJR Am J Roentgenol. 1977;128:549-561.Fein M, Fuchs KH, Bohrer T, et al. Fiberoptic technique for 24-hour bile reflux monitoring. Standards and normal values for gastric monitoring. Dig Dis Sci. 1996;41:216-225.Fuchs KH, DeMeester TR, Albertucci M. Specificity and sensitiv-ity of objective diagnosis of gastroesophageal reflux disease. Surgery. 1987;102:575-580.Iascone C, DeMeester TR, et al. Barrett’s esophagus: functional assessment, proposed pathogenesis, and surgical therapy. Arch Surg. 1983;118:543-549.Johnson LF, DeMeester TR. Development of 24-hour intra-esophageal pH monitoring composite scoring. J Clin Gastroenterol. 1986;8(suppl 1):52-58.Johnson LF, DeMeester TR. Twenty-four-hour pH monitoring of the |
Surgery_Schwartz_7257 | Surgery_Schwartz | LF, DeMeester TR. Development of 24-hour intra-esophageal pH monitoring composite scoring. J Clin Gastroenterol. 1986;8(suppl 1):52-58.Johnson LF, DeMeester TR. Twenty-four-hour pH monitoring of the distal esophagus: a quantitative measure of gastroesopha-geal reflux. Am J Gastroenterol. 1974;62(4):325-332.Kauer WK, Burdiles P, Ireland A, et al. Does duodenal juice reflux into the esophagus in patients with complicated GERD? Evaluation of a fiberoptic sensor for bilirubin. Am J Surg. 1995;169:98-103.Brunicardi_Ch25_p1009-p1098.indd 109101/03/19 6:06 PM 1092SPECIFIC CONSIDERATIONSPART IIKramer P, Hollander W. Comparison of experimental esopha-geal pain with clinical pain of angina pectoris and esophageal disease. Gastroenterology. 1955;29:719-743.Pandolfino JE, Richter JE, Ours T, et al. Ambulatory esophageal pH monitoring using a wireless system. Am J Gastroenterol. 2003;98:740-749.Reid BJ, Weinstein WM, Lewin KJ, et al. Endoscopic biopsy can detect high-grade dysplasia or early | Surgery_Schwartz. LF, DeMeester TR. Development of 24-hour intra-esophageal pH monitoring composite scoring. J Clin Gastroenterol. 1986;8(suppl 1):52-58.Johnson LF, DeMeester TR. Twenty-four-hour pH monitoring of the distal esophagus: a quantitative measure of gastroesopha-geal reflux. Am J Gastroenterol. 1974;62(4):325-332.Kauer WK, Burdiles P, Ireland A, et al. Does duodenal juice reflux into the esophagus in patients with complicated GERD? Evaluation of a fiberoptic sensor for bilirubin. Am J Surg. 1995;169:98-103.Brunicardi_Ch25_p1009-p1098.indd 109101/03/19 6:06 PM 1092SPECIFIC CONSIDERATIONSPART IIKramer P, Hollander W. Comparison of experimental esopha-geal pain with clinical pain of angina pectoris and esophageal disease. Gastroenterology. 1955;29:719-743.Pandolfino JE, Richter JE, Ours T, et al. Ambulatory esophageal pH monitoring using a wireless system. Am J Gastroenterol. 2003;98:740-749.Reid BJ, Weinstein WM, Lewin KJ, et al. Endoscopic biopsy can detect high-grade dysplasia or early |
Surgery_Schwartz_7258 | Surgery_Schwartz | al. Ambulatory esophageal pH monitoring using a wireless system. Am J Gastroenterol. 2003;98:740-749.Reid BJ, Weinstein WM, Lewin KJ, et al. Endoscopic biopsy can detect high-grade dysplasia or early adenocarcinoma in Barrett’s esophagus without grossly recognizable neoplastic lesions. Gastroenterology. 1988;94(1):81-90.Schwizer W, Hinder RA, DeMeester TR. Does delayed gastric emp-tying contribute to gastroesophageal reflux disease? Am J Surg. 1989;157:74-81.Stein HJ, DeMeester TR, et al. Three-dimensional imaging of the LES in gastroesophageal reflux disease. Ann Surg. 1991;214:374-384.Tutuian R, Vela MF, Balaji NS, et al. Esophageal function test-ing with combined multichannel intraluminal impedance and manometry; multicenter study in healthy volunteers. Clin Gastroenterol Hepatol. 2003;1:174-183.Wickremesinghe PC, Bayrit PQ, Manfredi OL, et al. Quantitative evaluation of bile diversion surgery utilizing 99mTc HIDA scin-tigraphy. Gastroenterology. 1983;84:354-363.Gastroesophageal | Surgery_Schwartz. al. Ambulatory esophageal pH monitoring using a wireless system. Am J Gastroenterol. 2003;98:740-749.Reid BJ, Weinstein WM, Lewin KJ, et al. Endoscopic biopsy can detect high-grade dysplasia or early adenocarcinoma in Barrett’s esophagus without grossly recognizable neoplastic lesions. Gastroenterology. 1988;94(1):81-90.Schwizer W, Hinder RA, DeMeester TR. Does delayed gastric emp-tying contribute to gastroesophageal reflux disease? Am J Surg. 1989;157:74-81.Stein HJ, DeMeester TR, et al. Three-dimensional imaging of the LES in gastroesophageal reflux disease. Ann Surg. 1991;214:374-384.Tutuian R, Vela MF, Balaji NS, et al. Esophageal function test-ing with combined multichannel intraluminal impedance and manometry; multicenter study in healthy volunteers. Clin Gastroenterol Hepatol. 2003;1:174-183.Wickremesinghe PC, Bayrit PQ, Manfredi OL, et al. Quantitative evaluation of bile diversion surgery utilizing 99mTc HIDA scin-tigraphy. Gastroenterology. 1983;84:354-363.Gastroesophageal |
Surgery_Schwartz_7259 | Surgery_Schwartz | PC, Bayrit PQ, Manfredi OL, et al. Quantitative evaluation of bile diversion surgery utilizing 99mTc HIDA scin-tigraphy. Gastroenterology. 1983;84:354-363.Gastroesophageal Reflux DiseaseAllison PR. Hiatus hernia: a 20 year retrospective survey. Ann Surg. 1973;178:273-276.Allison PR. Peptic ulcer of the esophagus. J Thorac Surg. 1946;15:308-317.Allison PR. Reflux esophagitis, sliding hiatus hernia and the anat-omy of repair. Surg Gynecol Obstet. 1951;92:419-431.Barlow AP, DeMeester TR, Ball CS, et al. The significance of the gastric secretory state in gastroesophageal reflux disease. Arch Surg. 1989;124:937-940.Bonavina L, DeMeester TR, McChesney L, Schwizer W, Albertucci M, Bailey RT. Drug-induced esophageal strictures. Ann Surg. 1987;206:173-183.Bremner RM, DeMeester TR, Crookes PF, et al. The effect of symp-toms and non-specific motility abnormalities on surgical therapy for gastroesophageal reflux disease. J Thorac Cardiovasc Surg. 1994;107:1244-1250.Castell DO. Nocturnal acid | Surgery_Schwartz. PC, Bayrit PQ, Manfredi OL, et al. Quantitative evaluation of bile diversion surgery utilizing 99mTc HIDA scin-tigraphy. Gastroenterology. 1983;84:354-363.Gastroesophageal Reflux DiseaseAllison PR. Hiatus hernia: a 20 year retrospective survey. Ann Surg. 1973;178:273-276.Allison PR. Peptic ulcer of the esophagus. J Thorac Surg. 1946;15:308-317.Allison PR. Reflux esophagitis, sliding hiatus hernia and the anat-omy of repair. Surg Gynecol Obstet. 1951;92:419-431.Barlow AP, DeMeester TR, Ball CS, et al. The significance of the gastric secretory state in gastroesophageal reflux disease. Arch Surg. 1989;124:937-940.Bonavina L, DeMeester TR, McChesney L, Schwizer W, Albertucci M, Bailey RT. Drug-induced esophageal strictures. Ann Surg. 1987;206:173-183.Bremner RM, DeMeester TR, Crookes PF, et al. The effect of symp-toms and non-specific motility abnormalities on surgical therapy for gastroesophageal reflux disease. J Thorac Cardiovasc Surg. 1994;107:1244-1250.Castell DO. Nocturnal acid |
Surgery_Schwartz_7260 | Surgery_Schwartz | et al. The effect of symp-toms and non-specific motility abnormalities on surgical therapy for gastroesophageal reflux disease. J Thorac Cardiovasc Surg. 1994;107:1244-1250.Castell DO. Nocturnal acid breakthrough in perspective: let’s not throw out the baby with the bathwater. Am J Gastroenterol. 2003;98:517-518.Chandrasoma P, Barrett N. So close, yet 50 years from the truth. J Gastrointest Surg. 1999;3:7-14.Clark GW, Ireland AP, Peters JH, Chandrasoma P, DeMeester TR, Bremner CG. Short segments of Barrett’s esophagus: a prevalent complication of gastroesophageal reflux disease with malignant potential. J Gastrointest Surg. 1997;1(2):113-122.DeMeester SR, Campos GM, DeMeester TR, et al. The impact of an antireflux procedure on intestinal metaplasia of the cardia. Ann Surg. 1998;228:547-556.DeMeester TR, Bonavina L, Albertucci M. Nissen fundoplication for gastroesophageal reflux disease: Evaluation of primary repair in 100 consecutive patients. Ann Surg. 1986;204:9-20.DeMeester TR, | Surgery_Schwartz. et al. The effect of symp-toms and non-specific motility abnormalities on surgical therapy for gastroesophageal reflux disease. J Thorac Cardiovasc Surg. 1994;107:1244-1250.Castell DO. Nocturnal acid breakthrough in perspective: let’s not throw out the baby with the bathwater. Am J Gastroenterol. 2003;98:517-518.Chandrasoma P, Barrett N. So close, yet 50 years from the truth. J Gastrointest Surg. 1999;3:7-14.Clark GW, Ireland AP, Peters JH, Chandrasoma P, DeMeester TR, Bremner CG. Short segments of Barrett’s esophagus: a prevalent complication of gastroesophageal reflux disease with malignant potential. J Gastrointest Surg. 1997;1(2):113-122.DeMeester SR, Campos GM, DeMeester TR, et al. The impact of an antireflux procedure on intestinal metaplasia of the cardia. Ann Surg. 1998;228:547-556.DeMeester TR, Bonavina L, Albertucci M. Nissen fundoplication for gastroesophageal reflux disease: Evaluation of primary repair in 100 consecutive patients. Ann Surg. 1986;204:9-20.DeMeester TR, |
Surgery_Schwartz_7261 | Surgery_Schwartz | TR, Bonavina L, Albertucci M. Nissen fundoplication for gastroesophageal reflux disease: Evaluation of primary repair in 100 consecutive patients. Ann Surg. 1986;204:9-20.DeMeester TR, Bonavina L, Iascone C, Courtney JV, Skinner DB. Chronic respiratory symptoms and occult gastroesophageal reflux. Ann Surg. 1990;211:337-345.DeMeester SR, DeMeester TR. Columnar mucosa and intesti-nal metaplasia of the esophagus: Fifty years of controversy. Ann Surg. 2000;231:303-321.DeMeester TR, Johansson KE, Franze I, et al. Indications, surgical technique, and long-term functional results of colon interposi-tion or bypass. Ann Surg. 1988;208:460-474.Desai KM, Klingensmith ME, Winslow ER, et al. Symptomatic out-comes of laparoscopic antireflux surgery in patients eligible for endoluminal therapies. Surg Endosc. 2002;16:1669-1673.Donahue PE, Samelson S, Nyhus LM, et al. The floppy Nissen fun-doplication: effective long-term control of pathologic reflux. Arch Surg. 1985;120:663-668.Farrell TM, | Surgery_Schwartz. TR, Bonavina L, Albertucci M. Nissen fundoplication for gastroesophageal reflux disease: Evaluation of primary repair in 100 consecutive patients. Ann Surg. 1986;204:9-20.DeMeester TR, Bonavina L, Iascone C, Courtney JV, Skinner DB. Chronic respiratory symptoms and occult gastroesophageal reflux. Ann Surg. 1990;211:337-345.DeMeester SR, DeMeester TR. Columnar mucosa and intesti-nal metaplasia of the esophagus: Fifty years of controversy. Ann Surg. 2000;231:303-321.DeMeester TR, Johansson KE, Franze I, et al. Indications, surgical technique, and long-term functional results of colon interposi-tion or bypass. Ann Surg. 1988;208:460-474.Desai KM, Klingensmith ME, Winslow ER, et al. Symptomatic out-comes of laparoscopic antireflux surgery in patients eligible for endoluminal therapies. Surg Endosc. 2002;16:1669-1673.Donahue PE, Samelson S, Nyhus LM, et al. The floppy Nissen fun-doplication: effective long-term control of pathologic reflux. Arch Surg. 1985;120:663-668.Farrell TM, |
Surgery_Schwartz_7262 | Surgery_Schwartz | Surg Endosc. 2002;16:1669-1673.Donahue PE, Samelson S, Nyhus LM, et al. The floppy Nissen fun-doplication: effective long-term control of pathologic reflux. Arch Surg. 1985;120:663-668.Farrell TM, Richardson WS, Halkar R, et al. Nissen fundoplication improves gastric motility in patients with delayed gastric emp-tying. Surg Endosc. 2001;15:271-274.Farrell TM, Richardson WS, Trus TL, et al. Response of atypical symptoms of gastroesophageal reflux antireflux surgery. Br J Surg. 2001;88:1649-1652.Farrell TM, Smith CD, Metreveli RE, et al. Fundoplication provides effective and durable symptom relief in patients with Barrett’s esophagus. Am J Surg. 1999;178:18-21.Fass R. Epidemiology and pathophysiology of symptomatic gastroesophageal reflux disease. Am J Gastroenterol. 2003;98 (3 suppl):S2-S7.Fiorucci S, Santucci L, Chiucchiú, Morelli A. Gastric acidity and gastroesophageal reflux patterns in patients with esophagitis. Gastroenterology. 1992;103:855-861.Fletcher J, Wirz A, Young J, et | Surgery_Schwartz. Surg Endosc. 2002;16:1669-1673.Donahue PE, Samelson S, Nyhus LM, et al. The floppy Nissen fun-doplication: effective long-term control of pathologic reflux. Arch Surg. 1985;120:663-668.Farrell TM, Richardson WS, Halkar R, et al. Nissen fundoplication improves gastric motility in patients with delayed gastric emp-tying. Surg Endosc. 2001;15:271-274.Farrell TM, Richardson WS, Trus TL, et al. Response of atypical symptoms of gastroesophageal reflux antireflux surgery. Br J Surg. 2001;88:1649-1652.Farrell TM, Smith CD, Metreveli RE, et al. Fundoplication provides effective and durable symptom relief in patients with Barrett’s esophagus. Am J Surg. 1999;178:18-21.Fass R. Epidemiology and pathophysiology of symptomatic gastroesophageal reflux disease. Am J Gastroenterol. 2003;98 (3 suppl):S2-S7.Fiorucci S, Santucci L, Chiucchiú, Morelli A. Gastric acidity and gastroesophageal reflux patterns in patients with esophagitis. Gastroenterology. 1992;103:855-861.Fletcher J, Wirz A, Young J, et |
Surgery_Schwartz_7263 | Surgery_Schwartz | S, Santucci L, Chiucchiú, Morelli A. Gastric acidity and gastroesophageal reflux patterns in patients with esophagitis. Gastroenterology. 1992;103:855-861.Fletcher J, Wirz A, Young J, et al. Unbuffered highly acidic gas-tric juice exists at the gastroesophageal junction after a meal. Gastroenterology. 2001;121:775-783.Fuchs KH, DeMeester TR, Hinder RA, et al. Computerized iden-tification of pathologic duodenogastric reflux using 24-hour gastric pH monitoring. Ann Surg. 1991;213:13-20.Gerson LB, Shetler K, Triadafilopoulos G. Prevalence of Barrett’s esophagus in asymptomatic individuals. Gastroenterology. 2002;123:461-467.Gillen P, Keeling P, Byrne PJ, et al. Implication of duodenogastric reflux in the pathogenesis of Barrett’s oesophagus. Br J Surg. 1988;75:540-543.Graham DY. The changing epidemiology of GERD: geography and Helicobacter pylori. Am J Gastroenterol. 2003;98:1462-1470.Gurski RR, Peters JH, Hagen JA, et al. Barrett’s esophagus can and does regress following antireflux | Surgery_Schwartz. S, Santucci L, Chiucchiú, Morelli A. Gastric acidity and gastroesophageal reflux patterns in patients with esophagitis. Gastroenterology. 1992;103:855-861.Fletcher J, Wirz A, Young J, et al. Unbuffered highly acidic gas-tric juice exists at the gastroesophageal junction after a meal. Gastroenterology. 2001;121:775-783.Fuchs KH, DeMeester TR, Hinder RA, et al. Computerized iden-tification of pathologic duodenogastric reflux using 24-hour gastric pH monitoring. Ann Surg. 1991;213:13-20.Gerson LB, Shetler K, Triadafilopoulos G. Prevalence of Barrett’s esophagus in asymptomatic individuals. Gastroenterology. 2002;123:461-467.Gillen P, Keeling P, Byrne PJ, et al. Implication of duodenogastric reflux in the pathogenesis of Barrett’s oesophagus. Br J Surg. 1988;75:540-543.Graham DY. The changing epidemiology of GERD: geography and Helicobacter pylori. Am J Gastroenterol. 2003;98:1462-1470.Gurski RR, Peters JH, Hagen JA, et al. Barrett’s esophagus can and does regress following antireflux |
Surgery_Schwartz_7264 | Surgery_Schwartz | epidemiology of GERD: geography and Helicobacter pylori. Am J Gastroenterol. 2003;98:1462-1470.Gurski RR, Peters JH, Hagen JA, et al. Barrett’s esophagus can and does regress following antireflux surgery: a study of prevalence and predictive features. J Am Coll Surg. 2003;196:706-712.Henderson RD, Henderson RF, Marryatt GV. Surgical management of 100 consecutive esophageal strictures. J Thorac Cardiovasc Surg. 1990;99:1-7.Hill LD, Kozarek RA, Kraemer SJ, et al. The gastroesophageal flap valve. In vitro and in vivo observations. Gastrointest Endosc. 1996;44(5):541-547.Hinder RA, Stein HJ, Bremner CG, et al. Relationship of a satisfac-tory outcome to normalization of delayed gastric emptying after Nissen fundoplication. Ann Surg. 1989;210:458-465.Hirota WK, Loughney TM, Lazas DJ, et al. Specialized intestinal metaplasia, dysplasia and cancer of the esophagus and esopha-gogastric junction: prevalence and clinical data. Gastroenterol-ogy. 1999;116(2):277-285.Hofstetter WA, Peters JH, | Surgery_Schwartz. epidemiology of GERD: geography and Helicobacter pylori. Am J Gastroenterol. 2003;98:1462-1470.Gurski RR, Peters JH, Hagen JA, et al. Barrett’s esophagus can and does regress following antireflux surgery: a study of prevalence and predictive features. J Am Coll Surg. 2003;196:706-712.Henderson RD, Henderson RF, Marryatt GV. Surgical management of 100 consecutive esophageal strictures. J Thorac Cardiovasc Surg. 1990;99:1-7.Hill LD, Kozarek RA, Kraemer SJ, et al. The gastroesophageal flap valve. In vitro and in vivo observations. Gastrointest Endosc. 1996;44(5):541-547.Hinder RA, Stein HJ, Bremner CG, et al. Relationship of a satisfac-tory outcome to normalization of delayed gastric emptying after Nissen fundoplication. Ann Surg. 1989;210:458-465.Hirota WK, Loughney TM, Lazas DJ, et al. Specialized intestinal metaplasia, dysplasia and cancer of the esophagus and esopha-gogastric junction: prevalence and clinical data. Gastroenterol-ogy. 1999;116(2):277-285.Hofstetter WA, Peters JH, |
Surgery_Schwartz_7265 | Surgery_Schwartz | Specialized intestinal metaplasia, dysplasia and cancer of the esophagus and esopha-gogastric junction: prevalence and clinical data. Gastroenterol-ogy. 1999;116(2):277-285.Hofstetter WA, Peters JH, DeMeester TR, et al. Long-term outcome of antireflux surgery in patients with Barrett’s esophagus. Ann Surg. 2001;234(4):532-538.Ireland AP, Clark GWB, DeMeester TR. Barrett’s esophagus: the significance of p53 in clinical practice. Ann Surg. 1997;225: 17-30.Isolauri J, Luostarinen M, Viljakka M, et al. Long-term compari-son of antireflux surgery versus conservative therapy for reflux esophagitis. Ann Surg. 1997;225:295-299.Jamieson JR, Hinder RA, DeMeester TR, et al. Analysis of 32 patients with Schatzki’s ring. Am J Surg. 1989;158:563-566.Johnson WE, Hagen JA, DeMeester TR, et al. Outcome of respira-tory symptoms after antireflux surgery on patients with gastro-esophageal reflux disease. Arch Surg. 1996;131:489-492.Kahrilas PJ. Diagnosis of symptomatic gastroesophageal reflux dis-ease. | Surgery_Schwartz. Specialized intestinal metaplasia, dysplasia and cancer of the esophagus and esopha-gogastric junction: prevalence and clinical data. Gastroenterol-ogy. 1999;116(2):277-285.Hofstetter WA, Peters JH, DeMeester TR, et al. Long-term outcome of antireflux surgery in patients with Barrett’s esophagus. Ann Surg. 2001;234(4):532-538.Ireland AP, Clark GWB, DeMeester TR. Barrett’s esophagus: the significance of p53 in clinical practice. Ann Surg. 1997;225: 17-30.Isolauri J, Luostarinen M, Viljakka M, et al. Long-term compari-son of antireflux surgery versus conservative therapy for reflux esophagitis. Ann Surg. 1997;225:295-299.Jamieson JR, Hinder RA, DeMeester TR, et al. Analysis of 32 patients with Schatzki’s ring. Am J Surg. 1989;158:563-566.Johnson WE, Hagen JA, DeMeester TR, et al. Outcome of respira-tory symptoms after antireflux surgery on patients with gastro-esophageal reflux disease. Arch Surg. 1996;131:489-492.Kahrilas PJ. Diagnosis of symptomatic gastroesophageal reflux dis-ease. |
Surgery_Schwartz_7266 | Surgery_Schwartz | respira-tory symptoms after antireflux surgery on patients with gastro-esophageal reflux disease. Arch Surg. 1996;131:489-492.Kahrilas PJ. Diagnosis of symptomatic gastroesophageal reflux dis-ease. Am J Gastroenterol. 2003;98:S15-S23.Kahrilas PJ. Radiofrequency therapy of the lower esophageal sphincter for treatment of GERD. Gastrointest Endosc. 2003;57:723-731.Brunicardi_Ch25_p1009-p1098.indd 109201/03/19 6:06 PM 1093ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Kaul BK, DeMeester TR, Oka M, et al. The cause of dysphagia in uncomplicated sliding hiatal hernia and its relief by hiatal her-niorrhaphy: a roentgenographic, manometric, and clinical study. Ann Surg. 1990;211:406-410.Khaitan L, Ray WA, Holzman MD, et al. Health care utilization after medical and surgical therapy for gastroesophageal reflux disease. Arch Surg. 2003;138:1356-1361.Labenz J, Tillenburg B, Peitz U, et al. Helicobacter pylori augments the pH-increasing effect of omeprazole in patients with duode-nal ulcer. | Surgery_Schwartz. respira-tory symptoms after antireflux surgery on patients with gastro-esophageal reflux disease. Arch Surg. 1996;131:489-492.Kahrilas PJ. Diagnosis of symptomatic gastroesophageal reflux dis-ease. Am J Gastroenterol. 2003;98:S15-S23.Kahrilas PJ. Radiofrequency therapy of the lower esophageal sphincter for treatment of GERD. Gastrointest Endosc. 2003;57:723-731.Brunicardi_Ch25_p1009-p1098.indd 109201/03/19 6:06 PM 1093ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Kaul BK, DeMeester TR, Oka M, et al. The cause of dysphagia in uncomplicated sliding hiatal hernia and its relief by hiatal her-niorrhaphy: a roentgenographic, manometric, and clinical study. Ann Surg. 1990;211:406-410.Khaitan L, Ray WA, Holzman MD, et al. Health care utilization after medical and surgical therapy for gastroesophageal reflux disease. Arch Surg. 2003;138:1356-1361.Labenz J, Tillenburg B, Peitz U, et al. Helicobacter pylori augments the pH-increasing effect of omeprazole in patients with duode-nal ulcer. |
Surgery_Schwartz_7267 | Surgery_Schwartz | reflux disease. Arch Surg. 2003;138:1356-1361.Labenz J, Tillenburg B, Peitz U, et al. Helicobacter pylori augments the pH-increasing effect of omeprazole in patients with duode-nal ulcer. Gastroenterology. 1996;110:725-732.Lin KM, Ueda RK, Hinder RA, et al. Etiology and importance of alkaline esophageal reflux. Am J Surg. 1991;162:553-557.Little AG, Ferguson MK, Skinner DB. Reoperation for failed anti-reflux operations. J Thorac Cardiovasc Surg. 1986;91:511-517.Liu JY, Finlayson SRG, Laycock WS, et al. Determining the appro-priate threshold for referral to surgery for gastroesophageal reflux disease. Surgery. 2003;133:5-12.Lundell L, Miettinen P, Myrvold HE, et al. Long-term management of gastrooesophageal reflux disease with omeprazole or open antireflux surgery: results of a prospective randomized trial. Eur J Gastroenterol Hepatol. 2000;12:879-887.Marshall RE, Anggiansah A, Owen WJ. Bile in the esopha-gus: clinical relevance and ambulatory detection. Br J Surg. | Surgery_Schwartz. reflux disease. Arch Surg. 2003;138:1356-1361.Labenz J, Tillenburg B, Peitz U, et al. Helicobacter pylori augments the pH-increasing effect of omeprazole in patients with duode-nal ulcer. Gastroenterology. 1996;110:725-732.Lin KM, Ueda RK, Hinder RA, et al. Etiology and importance of alkaline esophageal reflux. Am J Surg. 1991;162:553-557.Little AG, Ferguson MK, Skinner DB. Reoperation for failed anti-reflux operations. J Thorac Cardiovasc Surg. 1986;91:511-517.Liu JY, Finlayson SRG, Laycock WS, et al. Determining the appro-priate threshold for referral to surgery for gastroesophageal reflux disease. Surgery. 2003;133:5-12.Lundell L, Miettinen P, Myrvold HE, et al. Long-term management of gastrooesophageal reflux disease with omeprazole or open antireflux surgery: results of a prospective randomized trial. Eur J Gastroenterol Hepatol. 2000;12:879-887.Marshall RE, Anggiansah A, Owen WJ. Bile in the esopha-gus: clinical relevance and ambulatory detection. Br J Surg. |
Surgery_Schwartz_7268 | Surgery_Schwartz | of a prospective randomized trial. Eur J Gastroenterol Hepatol. 2000;12:879-887.Marshall RE, Anggiansah A, Owen WJ. Bile in the esopha-gus: clinical relevance and ambulatory detection. Br J Surg. 1997;84:21-28.Morgenthal CB, Shane MD, Stival A, et al. The durability of laparo-scopic Nissen fundoplication: 11-year outcomes. J Gastrointest Surg. 2007;11:693-700.Narayani RI, Burton MP, Young GS. Utility of esophageal biopsy in the diagnosis of non-erosive reflux disease. Dis Esophagus. 2003;16:187-192.Nissen R. Eine einfache operation zur beeinflussung der refluxo-esophagitis. Schweiz Med Wochenschr. 1956;86:590-592.Nissen R. Gastropexy and fundoplication in surgical treatment of hiatus hernia. Am J Dig Dis. 1961;6:954-961.Oberg S, Johansson H, Wenner J, et al. Endoscopic surveillance of columnar lined esophagus: frequency of intestinal meta-plasia detection and impact of antireflux surgery. Ann Surg. 2001;234:619-626.Orlando RC. The pathogenesis of gastroesophageal reflux disease: the | Surgery_Schwartz. of a prospective randomized trial. Eur J Gastroenterol Hepatol. 2000;12:879-887.Marshall RE, Anggiansah A, Owen WJ. Bile in the esopha-gus: clinical relevance and ambulatory detection. Br J Surg. 1997;84:21-28.Morgenthal CB, Shane MD, Stival A, et al. The durability of laparo-scopic Nissen fundoplication: 11-year outcomes. J Gastrointest Surg. 2007;11:693-700.Narayani RI, Burton MP, Young GS. Utility of esophageal biopsy in the diagnosis of non-erosive reflux disease. Dis Esophagus. 2003;16:187-192.Nissen R. Eine einfache operation zur beeinflussung der refluxo-esophagitis. Schweiz Med Wochenschr. 1956;86:590-592.Nissen R. Gastropexy and fundoplication in surgical treatment of hiatus hernia. Am J Dig Dis. 1961;6:954-961.Oberg S, Johansson H, Wenner J, et al. Endoscopic surveillance of columnar lined esophagus: frequency of intestinal meta-plasia detection and impact of antireflux surgery. Ann Surg. 2001;234:619-626.Orlando RC. The pathogenesis of gastroesophageal reflux disease: the |
Surgery_Schwartz_7269 | Surgery_Schwartz | lined esophagus: frequency of intestinal meta-plasia detection and impact of antireflux surgery. Ann Surg. 2001;234:619-626.Orlando RC. The pathogenesis of gastroesophageal reflux disease: the relationship between epithelial defense, dysmotility, and acid exposure. Am J Gastroenterol. 1997;92:3S-5S.Orringer MB, Skinner DB, Belsey RHR. Long-term results of the Mark IV operation for hiatal hernia and analyses of recur-rences and their treatment. J Thorac Cardiovasc Surg. 1972;63: 25-33.Parrilla P, Martinez de Haro LF, Ortiz A, et al. Long term results of a randomized prospective study comparing medical and sur-gical treatment in Barrett’s esophagus. Ann Surg. 2003;237: 291-298.Patti MG, Debas HT, Pellegrini CA. Esophageal manometry and 24-hour pH monitoring in the diagnosis of pulmonary aspiration secondary to gastroesophageal reflux. Am J Surg. 1992;163:401-406.Pearson FG, Cooper JD, Patterson GA, Ramirez J, Todd TR. Gastroplasty and fundoplication for complex reflux prob-lems. Ann | Surgery_Schwartz. lined esophagus: frequency of intestinal meta-plasia detection and impact of antireflux surgery. Ann Surg. 2001;234:619-626.Orlando RC. The pathogenesis of gastroesophageal reflux disease: the relationship between epithelial defense, dysmotility, and acid exposure. Am J Gastroenterol. 1997;92:3S-5S.Orringer MB, Skinner DB, Belsey RHR. Long-term results of the Mark IV operation for hiatal hernia and analyses of recur-rences and their treatment. J Thorac Cardiovasc Surg. 1972;63: 25-33.Parrilla P, Martinez de Haro LF, Ortiz A, et al. Long term results of a randomized prospective study comparing medical and sur-gical treatment in Barrett’s esophagus. Ann Surg. 2003;237: 291-298.Patti MG, Debas HT, Pellegrini CA. Esophageal manometry and 24-hour pH monitoring in the diagnosis of pulmonary aspiration secondary to gastroesophageal reflux. Am J Surg. 1992;163:401-406.Pearson FG, Cooper JD, Patterson GA, Ramirez J, Todd TR. Gastroplasty and fundoplication for complex reflux prob-lems. Ann |
Surgery_Schwartz_7270 | Surgery_Schwartz | aspiration secondary to gastroesophageal reflux. Am J Surg. 1992;163:401-406.Pearson FG, Cooper JD, Patterson GA, Ramirez J, Todd TR. Gastroplasty and fundoplication for complex reflux prob-lems. Ann Surg. 1987;206:473-481.Pelligrini CA, DeMeester TR, Johnson LF, et al. Gastroesophageal reflux and pulmonary aspiration: Incidence, functional abnor-mality, and results of surgical therapy. Surgery. 1979;86:110-119.Peters JH, Heimbucher J, Incarbone R, et al. Clinical and physi-ologic comparison of laparoscopic and open Nissen fundoplica-tion. J Am Coll Surg. 1995;180:385-393.Provenzale D, Kemp JA, Arora S, et al. A guide for surveillance of patients with Barrett’s esophagus. Am J Gastroenterol. 1994;89:670-680.Richter JE. Long-term management of gastroesophageal reflux disease and its complications. Am J Gastroenterol. 1997;92:30S-34S.Romagnuolo J, Meier MA, Sadowski DC. Medical or surgical ther-apy for erosive reflux esophagitis: Cost utility analysis using a Markov model. Ann Surg. | Surgery_Schwartz. aspiration secondary to gastroesophageal reflux. Am J Surg. 1992;163:401-406.Pearson FG, Cooper JD, Patterson GA, Ramirez J, Todd TR. Gastroplasty and fundoplication for complex reflux prob-lems. Ann Surg. 1987;206:473-481.Pelligrini CA, DeMeester TR, Johnson LF, et al. Gastroesophageal reflux and pulmonary aspiration: Incidence, functional abnor-mality, and results of surgical therapy. Surgery. 1979;86:110-119.Peters JH, Heimbucher J, Incarbone R, et al. Clinical and physi-ologic comparison of laparoscopic and open Nissen fundoplica-tion. J Am Coll Surg. 1995;180:385-393.Provenzale D, Kemp JA, Arora S, et al. A guide for surveillance of patients with Barrett’s esophagus. Am J Gastroenterol. 1994;89:670-680.Richter JE. Long-term management of gastroesophageal reflux disease and its complications. Am J Gastroenterol. 1997;92:30S-34S.Romagnuolo J, Meier MA, Sadowski DC. Medical or surgical ther-apy for erosive reflux esophagitis: Cost utility analysis using a Markov model. Ann Surg. |
Surgery_Schwartz_7271 | Surgery_Schwartz | Am J Gastroenterol. 1997;92:30S-34S.Romagnuolo J, Meier MA, Sadowski DC. Medical or surgical ther-apy for erosive reflux esophagitis: Cost utility analysis using a Markov model. Ann Surg. 2002;236:191-202.Schwizer W, Hinder RA, DeMeester TR. Does delayed gastric emp-tying contribute to gastroesophageal reflux disease? Am J Surg. 1989;157:74-81.Shaker R, Castell DO, Schoenfeld PS, Spechler SJ. Nighttime heart-burn is an underappreciated clinical problem that impacts sleep and daytime function: the results of a Gallup survey conducted on behalf of the American Gastroenterologic Association. Am J Gastroenterol. 2003;98:1487-1493.Siewert JR, Isolauri J, Feussuer M. Reoperation following failed fundoplication. World J Surg. 1989;13:791-796.Smith CD, McClusky DA, Rajhad MA, Lederman AB, Hunter JG. When fundoplication fails: redo? Ann Surg. 2005;241(6):861-871.Sontag SJ, O’Connell S, Khandelwal S, et al. Asthmatics with gastroesophageal reflux: long term results of a randomized trial of | Surgery_Schwartz. Am J Gastroenterol. 1997;92:30S-34S.Romagnuolo J, Meier MA, Sadowski DC. Medical or surgical ther-apy for erosive reflux esophagitis: Cost utility analysis using a Markov model. Ann Surg. 2002;236:191-202.Schwizer W, Hinder RA, DeMeester TR. Does delayed gastric emp-tying contribute to gastroesophageal reflux disease? Am J Surg. 1989;157:74-81.Shaker R, Castell DO, Schoenfeld PS, Spechler SJ. Nighttime heart-burn is an underappreciated clinical problem that impacts sleep and daytime function: the results of a Gallup survey conducted on behalf of the American Gastroenterologic Association. Am J Gastroenterol. 2003;98:1487-1493.Siewert JR, Isolauri J, Feussuer M. Reoperation following failed fundoplication. World J Surg. 1989;13:791-796.Smith CD, McClusky DA, Rajhad MA, Lederman AB, Hunter JG. When fundoplication fails: redo? Ann Surg. 2005;241(6):861-871.Sontag SJ, O’Connell S, Khandelwal S, et al. Asthmatics with gastroesophageal reflux: long term results of a randomized trial of |
Surgery_Schwartz_7272 | Surgery_Schwartz | JG. When fundoplication fails: redo? Ann Surg. 2005;241(6):861-871.Sontag SJ, O’Connell S, Khandelwal S, et al. Asthmatics with gastroesophageal reflux: long term results of a randomized trial of medical and surgical antireflux therapies. Am J Gastroenterol. 2003;98(5):987-999.Spechler SJ, Department of Veterans Affairs Gastroesophageal Reflux Disease Study Group. Comparison of medical and sur-gical therapy for complicated gastroesophageal reflux disease in veterans. N Engl J Med. 1992;326:786-792.Spechler SJ, Lee E, Ahmen D. Long term outcome of medical and surgical therapies for gastroesophageal reflux disease: follow-up of a randomized controlled trial. JAMA. 2001;285: 2331-2338.Spivak H, Farrell TM, Trus TL, et al. Laparoscopic fundoplication for dysphagia and peptic esophageal stricture. J Gastrointest Surg. 1998;2:555-560.Stein HJ, Barlow AP, DeMeester TR, Hinder RA. Complications of gastroesophageal reflux disease: role of the LES, esopha-geal acid and acid/alkaline exposure, | Surgery_Schwartz. JG. When fundoplication fails: redo? Ann Surg. 2005;241(6):861-871.Sontag SJ, O’Connell S, Khandelwal S, et al. Asthmatics with gastroesophageal reflux: long term results of a randomized trial of medical and surgical antireflux therapies. Am J Gastroenterol. 2003;98(5):987-999.Spechler SJ, Department of Veterans Affairs Gastroesophageal Reflux Disease Study Group. Comparison of medical and sur-gical therapy for complicated gastroesophageal reflux disease in veterans. N Engl J Med. 1992;326:786-792.Spechler SJ, Lee E, Ahmen D. Long term outcome of medical and surgical therapies for gastroesophageal reflux disease: follow-up of a randomized controlled trial. JAMA. 2001;285: 2331-2338.Spivak H, Farrell TM, Trus TL, et al. Laparoscopic fundoplication for dysphagia and peptic esophageal stricture. J Gastrointest Surg. 1998;2:555-560.Stein HJ, Barlow AP, DeMeester TR, Hinder RA. Complications of gastroesophageal reflux disease: role of the LES, esopha-geal acid and acid/alkaline exposure, |
Surgery_Schwartz_7273 | Surgery_Schwartz | J Gastrointest Surg. 1998;2:555-560.Stein HJ, Barlow AP, DeMeester TR, Hinder RA. Complications of gastroesophageal reflux disease: role of the LES, esopha-geal acid and acid/alkaline exposure, and duodenogastric reflux. Ann Surg. 1992;216(1):35-43.Stein HJ, Bremner RM, Jamieson J, DeMeester TR. Effect of Nissen fundoplication on esophageal motor function. Arch Surg. 1992;127:788-791.Terry M, Smith CD, Branum GD, et al. Outcomes of laparoscopic fundoplication for gastroesophageal reflux disease and parae-sophageal hernia: experience with 1000 consecutive cases. Surg Endosc. 2001;15:691-699.Terry ML, Vernon A, Hunter JG. Stapled-wedge Collis gastroplasty for the shortened esophagus. Am J Surg. 2004;188:195-199.Trus TL, Laycock WS, Waring JP, Branum GD, Hunter JG. Improvement in quality of life measures after laparo-scopic antireflux surgery. Ann Surg. 1999;229(3):331-336.Tseng D, Rizvi AZ, Fennerty MB, et al. Forty-eight-hour pH moni-toring increases sensitivity in detecting abnormal | Surgery_Schwartz. J Gastrointest Surg. 1998;2:555-560.Stein HJ, Barlow AP, DeMeester TR, Hinder RA. Complications of gastroesophageal reflux disease: role of the LES, esopha-geal acid and acid/alkaline exposure, and duodenogastric reflux. Ann Surg. 1992;216(1):35-43.Stein HJ, Bremner RM, Jamieson J, DeMeester TR. Effect of Nissen fundoplication on esophageal motor function. Arch Surg. 1992;127:788-791.Terry M, Smith CD, Branum GD, et al. Outcomes of laparoscopic fundoplication for gastroesophageal reflux disease and parae-sophageal hernia: experience with 1000 consecutive cases. Surg Endosc. 2001;15:691-699.Terry ML, Vernon A, Hunter JG. Stapled-wedge Collis gastroplasty for the shortened esophagus. Am J Surg. 2004;188:195-199.Trus TL, Laycock WS, Waring JP, Branum GD, Hunter JG. Improvement in quality of life measures after laparo-scopic antireflux surgery. Ann Surg. 1999;229(3):331-336.Tseng D, Rizvi AZ, Fennerty MB, et al. Forty-eight-hour pH moni-toring increases sensitivity in detecting abnormal |
Surgery_Schwartz_7274 | Surgery_Schwartz | life measures after laparo-scopic antireflux surgery. Ann Surg. 1999;229(3):331-336.Tseng D, Rizvi AZ, Fennerty MB, et al. Forty-eight-hour pH moni-toring increases sensitivity in detecting abnormal esophageal acid exposure. J Gastrointest Surg. 2005;9:1043-1052.Van Den Boom G, Go PM, Hameeetman W, et al. Cost effectiveness of medical versus surgical treatment in patients with severe or refractory gastroesophageal reflux disease in the Netherlands. Scand J Gastroenterol. 1996;31:1-9.Watson DI, Baigrie RJ, Jamieson GG. A learning curve for laparo-scopic fundoplication. Definable, avoidable, or a waste of time? Ann Surg. 1996;224:198-203.Wattchow DA, Jamieson GG, et al. Distribution of peptide-containing nerve fibers in the gastric musculature of patients undergoing sur-gery for gastroesophageal reflux. Ann Surg. 1992;290:153.Weston AP, Krmpotich P, Makdisi WF, et al. Short segment Barrett’s esophagus: clinical and histological features, associ-ated endoscopic findings, and association | Surgery_Schwartz. life measures after laparo-scopic antireflux surgery. Ann Surg. 1999;229(3):331-336.Tseng D, Rizvi AZ, Fennerty MB, et al. Forty-eight-hour pH moni-toring increases sensitivity in detecting abnormal esophageal acid exposure. J Gastrointest Surg. 2005;9:1043-1052.Van Den Boom G, Go PM, Hameeetman W, et al. Cost effectiveness of medical versus surgical treatment in patients with severe or refractory gastroesophageal reflux disease in the Netherlands. Scand J Gastroenterol. 1996;31:1-9.Watson DI, Baigrie RJ, Jamieson GG. A learning curve for laparo-scopic fundoplication. Definable, avoidable, or a waste of time? Ann Surg. 1996;224:198-203.Wattchow DA, Jamieson GG, et al. Distribution of peptide-containing nerve fibers in the gastric musculature of patients undergoing sur-gery for gastroesophageal reflux. Ann Surg. 1992;290:153.Weston AP, Krmpotich P, Makdisi WF, et al. Short segment Barrett’s esophagus: clinical and histological features, associ-ated endoscopic findings, and association |
Surgery_Schwartz_7275 | Surgery_Schwartz | reflux. Ann Surg. 1992;290:153.Weston AP, Krmpotich P, Makdisi WF, et al. Short segment Barrett’s esophagus: clinical and histological features, associ-ated endoscopic findings, and association with gastric intestinal metaplasia. Am J Gastroenterol. 1996;91:981-986.Williamson WA, Ellis FH Jr, Gibb SP, et al. Effect of antireflux oper-ation on Barrett’s mucosa. Ann Thorac Surg. 1990;49:537-541.Wright TA. High-grade dysplasia in Barrett’s oesophagus. Br J Surg. 1997;84:760-766.Brunicardi_Ch25_p1009-p1098.indd 109301/03/19 6:06 PM 1094SPECIFIC CONSIDERATIONSPART IIZaninotto G, DeMeester TR, Bremner CG, Smyrk TC, Cheng Shih-Chuan. Esophageal function in patients with reflux-induced strictures and its relevance to surgical treatment. Ann Thorac Surg. 1989;47:362-370.Diaphragmatic HerniasBombeck TC, Dillard DH, Nyhus LM. Muscular anatomy of the gastroesophageal junction and role of the phrenoesophageal ligament. Ann Surg. 1966;164:643-654.Casbella F, Sinanan M, Horgan S, Pellegrini | Surgery_Schwartz. reflux. Ann Surg. 1992;290:153.Weston AP, Krmpotich P, Makdisi WF, et al. Short segment Barrett’s esophagus: clinical and histological features, associ-ated endoscopic findings, and association with gastric intestinal metaplasia. Am J Gastroenterol. 1996;91:981-986.Williamson WA, Ellis FH Jr, Gibb SP, et al. Effect of antireflux oper-ation on Barrett’s mucosa. Ann Thorac Surg. 1990;49:537-541.Wright TA. High-grade dysplasia in Barrett’s oesophagus. Br J Surg. 1997;84:760-766.Brunicardi_Ch25_p1009-p1098.indd 109301/03/19 6:06 PM 1094SPECIFIC CONSIDERATIONSPART IIZaninotto G, DeMeester TR, Bremner CG, Smyrk TC, Cheng Shih-Chuan. Esophageal function in patients with reflux-induced strictures and its relevance to surgical treatment. Ann Thorac Surg. 1989;47:362-370.Diaphragmatic HerniasBombeck TC, Dillard DH, Nyhus LM. Muscular anatomy of the gastroesophageal junction and role of the phrenoesophageal ligament. Ann Surg. 1966;164:643-654.Casbella F, Sinanan M, Horgan S, Pellegrini |
Surgery_Schwartz_7276 | Surgery_Schwartz | TC, Dillard DH, Nyhus LM. Muscular anatomy of the gastroesophageal junction and role of the phrenoesophageal ligament. Ann Surg. 1966;164:643-654.Casbella F, Sinanan M, Horgan S, Pellegrini CA. Systematic use of gastric fundoplication in laparoscopic repair of paraesophageal hernias. Am J Surg. 1996;171:485-489.Dalgaard JB. Volvulus of the stomach. Acta Chir Scand. 1952;103:131-153.DeMeester TR, Lafontaine E, Joelsson BE, et al. The relation-ship of a hiatal hernia to the function of the body of the esophagus and the gastroesophageal junction. J Thorac Car-diovasc Surg. 1981;82:547-558.Eliska O. Phreno-oesophageal membrane and its role in the devel-opment of hiatal hernia. Acta Anat. 1973;86:137-150.Frantzides CT, Madan AK, Carlson MA, et al. A prospective, ran-domized trial of laparoscopic polytetrafluoroethylene (PTFE) patch repair vs simple cruroplasty for large hiatal hernia. Arch Surg. 2002;137:649-652.Fuller CB, Hagen JA, DeMeester TR, et al. The role of fundoplica-tion in the | Surgery_Schwartz. TC, Dillard DH, Nyhus LM. Muscular anatomy of the gastroesophageal junction and role of the phrenoesophageal ligament. Ann Surg. 1966;164:643-654.Casbella F, Sinanan M, Horgan S, Pellegrini CA. Systematic use of gastric fundoplication in laparoscopic repair of paraesophageal hernias. Am J Surg. 1996;171:485-489.Dalgaard JB. Volvulus of the stomach. Acta Chir Scand. 1952;103:131-153.DeMeester TR, Lafontaine E, Joelsson BE, et al. The relation-ship of a hiatal hernia to the function of the body of the esophagus and the gastroesophageal junction. J Thorac Car-diovasc Surg. 1981;82:547-558.Eliska O. Phreno-oesophageal membrane and its role in the devel-opment of hiatal hernia. Acta Anat. 1973;86:137-150.Frantzides CT, Madan AK, Carlson MA, et al. A prospective, ran-domized trial of laparoscopic polytetrafluoroethylene (PTFE) patch repair vs simple cruroplasty for large hiatal hernia. Arch Surg. 2002;137:649-652.Fuller CB, Hagen JA, DeMeester TR, et al. The role of fundoplica-tion in the |
Surgery_Schwartz_7277 | Surgery_Schwartz | polytetrafluoroethylene (PTFE) patch repair vs simple cruroplasty for large hiatal hernia. Arch Surg. 2002;137:649-652.Fuller CB, Hagen JA, DeMeester TR, et al. The role of fundoplica-tion in the treatment of type II paraesophageal hernia. J Thorac Cardiovasc Surg. 1996;111:655-661.Gangopadhyay N, Perrone JM, Soper NJ, et al. Outcomes of lapa-roscopic paraesophageal hernia repair in elderly and high-risk patients. Surgery. 2006;140:491-498; discussion 498.Granderath FA, Schweiger UM, Kamolz T, Asche KU, Pointner R. Laparoscopic Nissen fundoplication with prosthetic hiatal clo-sure reduces postoperative intrathoracic wrap herniation: pre-liminary results of a prospective randomized functional and clinical study. Arch Surg. 2005;140:40-48.Hashemi M, Peters JH, DeMeester TR, et al. Laparoscopic repair of large type III hiatal hernia: objective follow-up reveals high recurrence rate. J Am Coll Surg. 2000;190:539-560.Kahrilas PJ, Wu S, Lin S, Pouderoux P. Attenuation of esopha-geal | Surgery_Schwartz. polytetrafluoroethylene (PTFE) patch repair vs simple cruroplasty for large hiatal hernia. Arch Surg. 2002;137:649-652.Fuller CB, Hagen JA, DeMeester TR, et al. The role of fundoplica-tion in the treatment of type II paraesophageal hernia. J Thorac Cardiovasc Surg. 1996;111:655-661.Gangopadhyay N, Perrone JM, Soper NJ, et al. Outcomes of lapa-roscopic paraesophageal hernia repair in elderly and high-risk patients. Surgery. 2006;140:491-498; discussion 498.Granderath FA, Schweiger UM, Kamolz T, Asche KU, Pointner R. Laparoscopic Nissen fundoplication with prosthetic hiatal clo-sure reduces postoperative intrathoracic wrap herniation: pre-liminary results of a prospective randomized functional and clinical study. Arch Surg. 2005;140:40-48.Hashemi M, Peters JH, DeMeester TR, et al. Laparoscopic repair of large type III hiatal hernia: objective follow-up reveals high recurrence rate. J Am Coll Surg. 2000;190:539-560.Kahrilas PJ, Wu S, Lin S, Pouderoux P. Attenuation of esopha-geal |
Surgery_Schwartz_7278 | Surgery_Schwartz | repair of large type III hiatal hernia: objective follow-up reveals high recurrence rate. J Am Coll Surg. 2000;190:539-560.Kahrilas PJ, Wu S, Lin S, Pouderoux P. Attenuation of esopha-geal shortening during peristalsis with hiatus hernia. Gastro-enterology. 1995;109(6):1818-1825.Kleitsch WP. Embryology of congenital diaphragmatic hernia. I. Esophageal hiatus hernia. Arch Surg. 1958;76:868-873.Mattar SG, Bowers SP, Galloway KD, et al. Long-term outcome of laparoscopic repair of paraesophageal hernia. Surg Endosc. 2002;16:745-749.Menguy R. Surgical management of large paraesophageal hernia with complete intrathoracic stomach. World J Surg. 1988;12:415-422.Myers GA, Harms BA, Sarling JR. Management of paraesopha-geal hernia with a selective approach to antireflux surgery. Am J Surg. 1995;170:375-380.Oddsdottir M, Franco AL, Laycock WS, et al. Laparoscopic repair of paraesophageal hernia: New access, old technique. Surg Endosc. 1995;9:164-168.Oelschlager BK, Pellegrini CA, Hunter J, et | Surgery_Schwartz. repair of large type III hiatal hernia: objective follow-up reveals high recurrence rate. J Am Coll Surg. 2000;190:539-560.Kahrilas PJ, Wu S, Lin S, Pouderoux P. Attenuation of esopha-geal shortening during peristalsis with hiatus hernia. Gastro-enterology. 1995;109(6):1818-1825.Kleitsch WP. Embryology of congenital diaphragmatic hernia. I. Esophageal hiatus hernia. Arch Surg. 1958;76:868-873.Mattar SG, Bowers SP, Galloway KD, et al. Long-term outcome of laparoscopic repair of paraesophageal hernia. Surg Endosc. 2002;16:745-749.Menguy R. Surgical management of large paraesophageal hernia with complete intrathoracic stomach. World J Surg. 1988;12:415-422.Myers GA, Harms BA, Sarling JR. Management of paraesopha-geal hernia with a selective approach to antireflux surgery. Am J Surg. 1995;170:375-380.Oddsdottir M, Franco AL, Laycock WS, et al. Laparoscopic repair of paraesophageal hernia: New access, old technique. Surg Endosc. 1995;9:164-168.Oelschlager BK, Pellegrini CA, Hunter J, et |
Surgery_Schwartz_7279 | Surgery_Schwartz | M, Franco AL, Laycock WS, et al. Laparoscopic repair of paraesophageal hernia: New access, old technique. Surg Endosc. 1995;9:164-168.Oelschlager BK, Pellegrini CA, Hunter J, et al. Biologic pros-thesis reduces recurrence after laparoscopic paraesophageal hernia repair: a multicenter, prospective, randomized trial. Ann Surg. 2006;244(4):481-490.Patti MG, Goldberg HI, Arcerito M, Bortolasi L, Tong J, Way LW. Hiatal hernia size affects LES function, esophageal acid exposure, and the degree of mucosal injury. Am J Surg. 1996;171(1):182-186.Pierre AF, Luketich JD, Fernando HC, et al. Results of laparo-scopic repair of giant paraesophageal hernias: 200 consecutive patients. Ann Thorac Surg. 2002;74:1909-1915.Skinner DB, Belsey RH. Surgical management of esophageal reflux and hiatus hernia: long-term results with 1030 patients. J Thorac Cardiovasc Surg. 1967;53:33-54.Stylopoulos N, Gazelle GS, Ratner DW. Paraesophageal hernias: operation or observation. Ann Surg. 2002;236:492-500.Trus TL, | Surgery_Schwartz. M, Franco AL, Laycock WS, et al. Laparoscopic repair of paraesophageal hernia: New access, old technique. Surg Endosc. 1995;9:164-168.Oelschlager BK, Pellegrini CA, Hunter J, et al. Biologic pros-thesis reduces recurrence after laparoscopic paraesophageal hernia repair: a multicenter, prospective, randomized trial. Ann Surg. 2006;244(4):481-490.Patti MG, Goldberg HI, Arcerito M, Bortolasi L, Tong J, Way LW. Hiatal hernia size affects LES function, esophageal acid exposure, and the degree of mucosal injury. Am J Surg. 1996;171(1):182-186.Pierre AF, Luketich JD, Fernando HC, et al. Results of laparo-scopic repair of giant paraesophageal hernias: 200 consecutive patients. Ann Thorac Surg. 2002;74:1909-1915.Skinner DB, Belsey RH. Surgical management of esophageal reflux and hiatus hernia: long-term results with 1030 patients. J Thorac Cardiovasc Surg. 1967;53:33-54.Stylopoulos N, Gazelle GS, Ratner DW. Paraesophageal hernias: operation or observation. Ann Surg. 2002;236:492-500.Trus TL, |
Surgery_Schwartz_7280 | Surgery_Schwartz | results with 1030 patients. J Thorac Cardiovasc Surg. 1967;53:33-54.Stylopoulos N, Gazelle GS, Ratner DW. Paraesophageal hernias: operation or observation. Ann Surg. 2002;236:492-500.Trus TL, Bax T, Richardson WS, et al. Complications of lapa-roscopic paraesophageal hernia repair. J Gastrointest Surg. 1997;1(3):221-227; discussion 228.Wo JM, Branum GD, Hunter JG, et al. Clinical features of type III (mixed) paraesophageal hernia. Am J Gastroenterol. 1996;91:914-916.Miscellaneous Esophageal LesionsBurdick JS, Venu RP, Hogan WJ. Cutting the defiant lower esopha-geal ring. Gastrointest Endosc. 1993;39:616-619.Burt M, Diehl W, Martini N, et al. Malignant esophagorespiratory fistula: management options and survival. Ann Thorac Surg. 1991;52:1222-1228.Chen MYM, Ott DJ, Donati DL. Correlation of lower esophageal mucosal ring and LES pressure. Dig Dis Sci. 1994;39:766-769.D’Haens G, Rutgeerts P, Geboes K, et al. The natural history of esophageal Crohn’s disease. Three patterns of evolution. | Surgery_Schwartz. results with 1030 patients. J Thorac Cardiovasc Surg. 1967;53:33-54.Stylopoulos N, Gazelle GS, Ratner DW. Paraesophageal hernias: operation or observation. Ann Surg. 2002;236:492-500.Trus TL, Bax T, Richardson WS, et al. Complications of lapa-roscopic paraesophageal hernia repair. J Gastrointest Surg. 1997;1(3):221-227; discussion 228.Wo JM, Branum GD, Hunter JG, et al. Clinical features of type III (mixed) paraesophageal hernia. Am J Gastroenterol. 1996;91:914-916.Miscellaneous Esophageal LesionsBurdick JS, Venu RP, Hogan WJ. Cutting the defiant lower esopha-geal ring. Gastrointest Endosc. 1993;39:616-619.Burt M, Diehl W, Martini N, et al. Malignant esophagorespiratory fistula: management options and survival. Ann Thorac Surg. 1991;52:1222-1228.Chen MYM, Ott DJ, Donati DL. Correlation of lower esophageal mucosal ring and LES pressure. Dig Dis Sci. 1994;39:766-769.D’Haens G, Rutgeerts P, Geboes K, et al. The natural history of esophageal Crohn’s disease. Three patterns of evolution. |
Surgery_Schwartz_7281 | Surgery_Schwartz | lower esophageal mucosal ring and LES pressure. Dig Dis Sci. 1994;39:766-769.D’Haens G, Rutgeerts P, Geboes K, et al. The natural history of esophageal Crohn’s disease. Three patterns of evolution. Gastrointest Endosc. 1994;40:296-300.Eckhardt VF, Kanzler G, Willems D. Single dilation of symptom-atic Schatzki rings. A prospective evaluation of its effectiveness. Dig Dis Sci. 1992;37:577-582.Klein HA, Wald A, Graham TO, et al. Comparative studies of esophageal function in systemic sclerosis. Gastroenterology. 1992;102:1551-1556.Mathisen DJ, Grillo HC, Wain JC, et al. Management of acquired nonmalignant tracheoesophageal fistula. Ann Thorac Surg. 1991;52:759-765.Poirier NC, Taillefer R, Topart P, Duranceau A. Antireflux opera-tions in patients with scleroderma. Ann Thorac Surg. 1994; 58:66-72.Soudah HC, Hasler WL, Owyang C. Effect of octreotide on intesti-nal motility and bacterial overgrowth in scleroderma. N Engl J Med. 1991;325:1461-1467.Toskes PP. Hope for the treatment of | Surgery_Schwartz. lower esophageal mucosal ring and LES pressure. Dig Dis Sci. 1994;39:766-769.D’Haens G, Rutgeerts P, Geboes K, et al. The natural history of esophageal Crohn’s disease. Three patterns of evolution. Gastrointest Endosc. 1994;40:296-300.Eckhardt VF, Kanzler G, Willems D. Single dilation of symptom-atic Schatzki rings. A prospective evaluation of its effectiveness. Dig Dis Sci. 1992;37:577-582.Klein HA, Wald A, Graham TO, et al. Comparative studies of esophageal function in systemic sclerosis. Gastroenterology. 1992;102:1551-1556.Mathisen DJ, Grillo HC, Wain JC, et al. Management of acquired nonmalignant tracheoesophageal fistula. Ann Thorac Surg. 1991;52:759-765.Poirier NC, Taillefer R, Topart P, Duranceau A. Antireflux opera-tions in patients with scleroderma. Ann Thorac Surg. 1994; 58:66-72.Soudah HC, Hasler WL, Owyang C. Effect of octreotide on intesti-nal motility and bacterial overgrowth in scleroderma. N Engl J Med. 1991;325:1461-1467.Toskes PP. Hope for the treatment of |
Surgery_Schwartz_7282 | Surgery_Schwartz | 58:66-72.Soudah HC, Hasler WL, Owyang C. Effect of octreotide on intesti-nal motility and bacterial overgrowth in scleroderma. N Engl J Med. 1991;325:1461-1467.Toskes PP. Hope for the treatment of intestinal scleroderma (Letter to the Editor). N Engl J Med. 1991;325:1508.Wilcox CM, Straub RF. Prospective endoscopic characterization of cytomegalovirus esophagitis in AIDS. Gastrointest Endosc. 1994;40:481-484.Motility Disorders of the Pharynx and EsophagusAchem SR, Crittenden J, Kolts B, et al. Long-term clinical and manometric follow-up of patients with nonspecific esophageal motor disorders. Am J Gastroenterol. 1992;87:825-830.Andreollo NA, Earlam RJ. Heller’s myotomy for achalasia: is an added antireflux procedure necessary? Br J Surg. 1987;74:765-769.Anselmino M, Perdikis G, Hinder RA, et al. Heller myotomy is superior to dilatation for the treatment of early achalasia. Arch Surg. 1997;132:233-240.Bianco A, Cagossi M, Scrimieri D, et al. Appearance of esopha-geal peristalsis in | Surgery_Schwartz. 58:66-72.Soudah HC, Hasler WL, Owyang C. Effect of octreotide on intesti-nal motility and bacterial overgrowth in scleroderma. N Engl J Med. 1991;325:1461-1467.Toskes PP. Hope for the treatment of intestinal scleroderma (Letter to the Editor). N Engl J Med. 1991;325:1508.Wilcox CM, Straub RF. Prospective endoscopic characterization of cytomegalovirus esophagitis in AIDS. Gastrointest Endosc. 1994;40:481-484.Motility Disorders of the Pharynx and EsophagusAchem SR, Crittenden J, Kolts B, et al. Long-term clinical and manometric follow-up of patients with nonspecific esophageal motor disorders. Am J Gastroenterol. 1992;87:825-830.Andreollo NA, Earlam RJ. Heller’s myotomy for achalasia: is an added antireflux procedure necessary? Br J Surg. 1987;74:765-769.Anselmino M, Perdikis G, Hinder RA, et al. Heller myotomy is superior to dilatation for the treatment of early achalasia. Arch Surg. 1997;132:233-240.Bianco A, Cagossi M, Scrimieri D, et al. Appearance of esopha-geal peristalsis in |
Surgery_Schwartz_7283 | Surgery_Schwartz | RA, et al. Heller myotomy is superior to dilatation for the treatment of early achalasia. Arch Surg. 1997;132:233-240.Bianco A, Cagossi M, Scrimieri D, et al. Appearance of esopha-geal peristalsis in treated idiopathic achalasia. Dig Dis Sci. 1986;90:978-983.Bonavina L, Nosadinia A, Bardini R, Baessato M, Peracchia A. Primary treatment of esophageal achalasia: long-term results of myotomy and Dor fundoplication. Arch Surg. 1992;127:222-226.Chen LQ, Chughtau T, Sideris L, et al. Long term effects of myotomy and partial fundoplication for esophageal achalasia. Dis Esophagus. 2002;15:171-179.Code CF, Schlegel JF, Kelley ML, et al. Hypertensive gastroesopha-geal sphincter. Mayo Clin Proc. 1960;35:391-399.Cook IJ, Blumbergs P, Cash K, Jamieson GG, Shearman DJ. Struc-tural abnormalities of the cricopharyngeus muscle in patients with pharyngeal (Zenker’s) diverticulum. J Gastroenterol Hepatol. 1992;7:556-562.Brunicardi_Ch25_p1009-p1098.indd 109401/03/19 6:06 PM 1095ESOPHAGUS AND | Surgery_Schwartz. RA, et al. Heller myotomy is superior to dilatation for the treatment of early achalasia. Arch Surg. 1997;132:233-240.Bianco A, Cagossi M, Scrimieri D, et al. Appearance of esopha-geal peristalsis in treated idiopathic achalasia. Dig Dis Sci. 1986;90:978-983.Bonavina L, Nosadinia A, Bardini R, Baessato M, Peracchia A. Primary treatment of esophageal achalasia: long-term results of myotomy and Dor fundoplication. Arch Surg. 1992;127:222-226.Chen LQ, Chughtau T, Sideris L, et al. Long term effects of myotomy and partial fundoplication for esophageal achalasia. Dis Esophagus. 2002;15:171-179.Code CF, Schlegel JF, Kelley ML, et al. Hypertensive gastroesopha-geal sphincter. Mayo Clin Proc. 1960;35:391-399.Cook IJ, Blumbergs P, Cash K, Jamieson GG, Shearman DJ. Struc-tural abnormalities of the cricopharyngeus muscle in patients with pharyngeal (Zenker’s) diverticulum. J Gastroenterol Hepatol. 1992;7:556-562.Brunicardi_Ch25_p1009-p1098.indd 109401/03/19 6:06 PM 1095ESOPHAGUS AND |
Surgery_Schwartz_7284 | Surgery_Schwartz | of the cricopharyngeus muscle in patients with pharyngeal (Zenker’s) diverticulum. J Gastroenterol Hepatol. 1992;7:556-562.Brunicardi_Ch25_p1009-p1098.indd 109401/03/19 6:06 PM 1095ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Cook IJ, Gabb M, Panagopoulos V, et al. Pharyngeal (Zenker’s) diverticulum is a disorder of upper esophageal sphincter open-ing. Gastroenterology. 1992;103:1229-1235.Csendes A, Braghetto I, Henríquez A, Cortés C. Late results of a prospective randomized study comparing forceful dilata-tion and oesophagomyotomy in patients with achalasia. Gut. 1989;30(3):299-304.DeMeester TR, Johansson KE, Franze I, et al. Indications, surgical technique, and long-term functional results of colon interposi-tion or bypass. Ann Surg. 1988;208:460-474.DeMeester TR, Lafontaine E, et al. The relationship of a hia-tal hernia to the function of the body of the esophagus and the gastroesophageal junction. J Thorac Cardiovasc Surg. 1981;82:547-558.Eckardt V, Aignherr C, Bernhard G. | Surgery_Schwartz. of the cricopharyngeus muscle in patients with pharyngeal (Zenker’s) diverticulum. J Gastroenterol Hepatol. 1992;7:556-562.Brunicardi_Ch25_p1009-p1098.indd 109401/03/19 6:06 PM 1095ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Cook IJ, Gabb M, Panagopoulos V, et al. Pharyngeal (Zenker’s) diverticulum is a disorder of upper esophageal sphincter open-ing. Gastroenterology. 1992;103:1229-1235.Csendes A, Braghetto I, Henríquez A, Cortés C. Late results of a prospective randomized study comparing forceful dilata-tion and oesophagomyotomy in patients with achalasia. Gut. 1989;30(3):299-304.DeMeester TR, Johansson KE, Franze I, et al. Indications, surgical technique, and long-term functional results of colon interposi-tion or bypass. Ann Surg. 1988;208:460-474.DeMeester TR, Lafontaine E, et al. The relationship of a hia-tal hernia to the function of the body of the esophagus and the gastroesophageal junction. J Thorac Cardiovasc Surg. 1981;82:547-558.Eckardt V, Aignherr C, Bernhard G. |
Surgery_Schwartz_7285 | Surgery_Schwartz | al. The relationship of a hia-tal hernia to the function of the body of the esophagus and the gastroesophageal junction. J Thorac Cardiovasc Surg. 1981;82:547-558.Eckardt V, Aignherr C, Bernhard G. Predictors of outcome in patients with achalasia treated by pneumatic dilation. Gastroenterology. 1992;103(6):1732-1738.Ekberg O, Wahlgren L. Dysfunction of pharyngeal swallowing: a cineradiographic investigation in 854 dysphagial patients. Acta Radiol Diagn. 1985;26:389-395.Ellis FH. Long esophagomyotomy for diffuse esophageal spasm and related disorders: An historical overview. Dis Esophagus. 1998;11:210-214.Ellis FH Jr. Oesophagomyotomy for achalasia: a 22-year experi-ence. Br J Surg. 1993;80:882-885.Evander A, Little AG, et al. Diverticula of the mid and lower esoph-agus. World J Surg. 1986;10:820-828.Ferguson TB, Woodbury JD, Roper CL. Giant muscular hypertro-phy of the esophagus. Ann Thorac Surg. 1969;8:209-218.Foker JE, Ring WE, Varco RL. Technique of jejunal interposi-tion for | Surgery_Schwartz. al. The relationship of a hia-tal hernia to the function of the body of the esophagus and the gastroesophageal junction. J Thorac Cardiovasc Surg. 1981;82:547-558.Eckardt V, Aignherr C, Bernhard G. Predictors of outcome in patients with achalasia treated by pneumatic dilation. Gastroenterology. 1992;103(6):1732-1738.Ekberg O, Wahlgren L. Dysfunction of pharyngeal swallowing: a cineradiographic investigation in 854 dysphagial patients. Acta Radiol Diagn. 1985;26:389-395.Ellis FH. Long esophagomyotomy for diffuse esophageal spasm and related disorders: An historical overview. Dis Esophagus. 1998;11:210-214.Ellis FH Jr. Oesophagomyotomy for achalasia: a 22-year experi-ence. Br J Surg. 1993;80:882-885.Evander A, Little AG, et al. Diverticula of the mid and lower esoph-agus. World J Surg. 1986;10:820-828.Ferguson TB, Woodbury JD, Roper CL. Giant muscular hypertro-phy of the esophagus. Ann Thorac Surg. 1969;8:209-218.Foker JE, Ring WE, Varco RL. Technique of jejunal interposi-tion for |
Surgery_Schwartz_7286 | Surgery_Schwartz | 1986;10:820-828.Ferguson TB, Woodbury JD, Roper CL. Giant muscular hypertro-phy of the esophagus. Ann Thorac Surg. 1969;8:209-218.Foker JE, Ring WE, Varco RL. Technique of jejunal interposi-tion for esophageal replacement. J Thorac Cardiovasc Surg. 1982;83:928-933.Gutschow CA, Hamoir M, Rombaux P, et al. Management of pha-ryngoesophageal (Zenker’s) diverticulum: which technique? Ann Thorac Surg. 2002;74:1677-1682.Hirano I, Tatum RP, Shi G, et al. Manometric heterogene-ity in patients with idiopathic achalasia. Gastroenterology. 2001;120:789-798.Jeansonne LO, White BC, Pilger KE, et al. Ten-year follow-up of laparoscopic Heller myotomy for achalasia shows durability. Surg Endosc. 2007;21:1498-1502.Jobe BA, Kim CY, Minjarez RC, et al. Simplifying minimally invasive transhiatal esophagectomy with the inversion approach: Lessons learned from the first 20 cases. Arch Surg. 2006;141:857-865; discussion 865.Kahrilas PJ, Logemann JA, Lin S, Ergun GA. Pharyngeal clearance during swallowing: a | Surgery_Schwartz. 1986;10:820-828.Ferguson TB, Woodbury JD, Roper CL. Giant muscular hypertro-phy of the esophagus. Ann Thorac Surg. 1969;8:209-218.Foker JE, Ring WE, Varco RL. Technique of jejunal interposi-tion for esophageal replacement. J Thorac Cardiovasc Surg. 1982;83:928-933.Gutschow CA, Hamoir M, Rombaux P, et al. Management of pha-ryngoesophageal (Zenker’s) diverticulum: which technique? Ann Thorac Surg. 2002;74:1677-1682.Hirano I, Tatum RP, Shi G, et al. Manometric heterogene-ity in patients with idiopathic achalasia. Gastroenterology. 2001;120:789-798.Jeansonne LO, White BC, Pilger KE, et al. Ten-year follow-up of laparoscopic Heller myotomy for achalasia shows durability. Surg Endosc. 2007;21:1498-1502.Jobe BA, Kim CY, Minjarez RC, et al. Simplifying minimally invasive transhiatal esophagectomy with the inversion approach: Lessons learned from the first 20 cases. Arch Surg. 2006;141:857-865; discussion 865.Kahrilas PJ, Logemann JA, Lin S, Ergun GA. Pharyngeal clearance during swallowing: a |
Surgery_Schwartz_7287 | Surgery_Schwartz | with the inversion approach: Lessons learned from the first 20 cases. Arch Surg. 2006;141:857-865; discussion 865.Kahrilas PJ, Logemann JA, Lin S, Ergun GA. Pharyngeal clearance during swallowing: a combined manometric and videofluoro-scopic study. Gastroenterology. 1992;103(1):128-136.Kostic S, Kjellin A, Ruth M, et al. Pneumatic dilation or laparo-scopic cardiomyotomy in the management of newly diagnosed idiopathic achalasia. Results of a randomized controlled trial. World J Surg. 2007;31:470-478.Lam HG, Dekker W, Kan G, et al. Acute noncardiac chest pain in a coronary care unit. Gastroenterology. 1992;102:453-460.Mellow MH. Return of esophageal peristalsis in idiopathic achala-sia. Gastroenterology. 1976;70:1148-1151.Meshkinpour H, Haghighat P, Meshkinpour A. Quality of life among patients treated for achalasia. Dig Dis Sci. 1996;41(2):352-356.Migliore M, Payne H, Jeyasingham K. Pathophysiologic basis for operation on Zenker’s diverticulum. Ann Thorac Surg. 1994;57:1616-1621.Moser | Surgery_Schwartz. with the inversion approach: Lessons learned from the first 20 cases. Arch Surg. 2006;141:857-865; discussion 865.Kahrilas PJ, Logemann JA, Lin S, Ergun GA. Pharyngeal clearance during swallowing: a combined manometric and videofluoro-scopic study. Gastroenterology. 1992;103(1):128-136.Kostic S, Kjellin A, Ruth M, et al. Pneumatic dilation or laparo-scopic cardiomyotomy in the management of newly diagnosed idiopathic achalasia. Results of a randomized controlled trial. World J Surg. 2007;31:470-478.Lam HG, Dekker W, Kan G, et al. Acute noncardiac chest pain in a coronary care unit. Gastroenterology. 1992;102:453-460.Mellow MH. Return of esophageal peristalsis in idiopathic achala-sia. Gastroenterology. 1976;70:1148-1151.Meshkinpour H, Haghighat P, Meshkinpour A. Quality of life among patients treated for achalasia. Dig Dis Sci. 1996;41(2):352-356.Migliore M, Payne H, Jeyasingham K. Pathophysiologic basis for operation on Zenker’s diverticulum. Ann Thorac Surg. 1994;57:1616-1621.Moser |
Surgery_Schwartz_7288 | Surgery_Schwartz | treated for achalasia. Dig Dis Sci. 1996;41(2):352-356.Migliore M, Payne H, Jeyasingham K. Pathophysiologic basis for operation on Zenker’s diverticulum. Ann Thorac Surg. 1994;57:1616-1621.Moser G, Vacariu-Granser GV, Schneider C, et al. High incidence of esophageal motor disorders in consecutive patients with glo-bus sensation. Gastroenterology. 1991;101:1512-1521.Moses PL, Ellis LM, Anees MR, et al. Antineural antibodies in idiopathic achalasia and gastro-oesophageal reflux disease. Gut. 2003;52:629-636.Nehra D, Lord RV, DeMeester TR, et al. Physiologic basis for the treatment of epiphrenic diverticulum. Ann Surg. 2002;235: 346-354.Oelschlager BK, Chang L, Pellegrini CA. Improved outcome after extended gastric myotomy for achalasia. Arch Surg. 2003;138(5):490-495.O’Rourke RW, Seltman AK, Chang EY, et al. A model for gastric banding in the treatment of morbid obesity: the effect of chronic partial gastric outlet obstruction on esophageal physiology. Ann Surg. 2006;244:723-733.Patti | Surgery_Schwartz. treated for achalasia. Dig Dis Sci. 1996;41(2):352-356.Migliore M, Payne H, Jeyasingham K. Pathophysiologic basis for operation on Zenker’s diverticulum. Ann Thorac Surg. 1994;57:1616-1621.Moser G, Vacariu-Granser GV, Schneider C, et al. High incidence of esophageal motor disorders in consecutive patients with glo-bus sensation. Gastroenterology. 1991;101:1512-1521.Moses PL, Ellis LM, Anees MR, et al. Antineural antibodies in idiopathic achalasia and gastro-oesophageal reflux disease. Gut. 2003;52:629-636.Nehra D, Lord RV, DeMeester TR, et al. Physiologic basis for the treatment of epiphrenic diverticulum. Ann Surg. 2002;235: 346-354.Oelschlager BK, Chang L, Pellegrini CA. Improved outcome after extended gastric myotomy for achalasia. Arch Surg. 2003;138(5):490-495.O’Rourke RW, Seltman AK, Chang EY, et al. A model for gastric banding in the treatment of morbid obesity: the effect of chronic partial gastric outlet obstruction on esophageal physiology. Ann Surg. 2006;244:723-733.Patti |
Surgery_Schwartz_7289 | Surgery_Schwartz | Chang EY, et al. A model for gastric banding in the treatment of morbid obesity: the effect of chronic partial gastric outlet obstruction on esophageal physiology. Ann Surg. 2006;244:723-733.Patti MG, Fisichella PM, Peretta S, et al. Impact of minimally invasive surgery on the treatment of esophageal achalasia: a decade of change. J Am Coll Surg. 2003;196:698-703.Pellegrini C, Wetter LA, Patti M, et al. Thoracoscopic esophagomy-otomy: initial experience with a new approach for the treatment of achalasia. Ann Surg. 1992;216:291-299.Peters JH. An antireflux procedure is critical to the long-term out-come of esophageal myotomy for achalasia. J Gastrointest Surg. 2001;5:17-20.Peters JH, Kauer WK, Ireland AP, et al. Esophageal resection with colon interposition for end-stage achalasia. Arch Surg. 1995;130:632-636.Ponce J, Garrigues V, Pertejo V, et al. Individual prediction of response to pneumatic dilation in patients with achalasia. Dig Dis Sci. 1996;41:2135-2141.Richards WO, Torquati A, | Surgery_Schwartz. Chang EY, et al. A model for gastric banding in the treatment of morbid obesity: the effect of chronic partial gastric outlet obstruction on esophageal physiology. Ann Surg. 2006;244:723-733.Patti MG, Fisichella PM, Peretta S, et al. Impact of minimally invasive surgery on the treatment of esophageal achalasia: a decade of change. J Am Coll Surg. 2003;196:698-703.Pellegrini C, Wetter LA, Patti M, et al. Thoracoscopic esophagomy-otomy: initial experience with a new approach for the treatment of achalasia. Ann Surg. 1992;216:291-299.Peters JH. An antireflux procedure is critical to the long-term out-come of esophageal myotomy for achalasia. J Gastrointest Surg. 2001;5:17-20.Peters JH, Kauer WK, Ireland AP, et al. Esophageal resection with colon interposition for end-stage achalasia. Arch Surg. 1995;130:632-636.Ponce J, Garrigues V, Pertejo V, et al. Individual prediction of response to pneumatic dilation in patients with achalasia. Dig Dis Sci. 1996;41:2135-2141.Richards WO, Torquati A, |
Surgery_Schwartz_7290 | Surgery_Schwartz | 1995;130:632-636.Ponce J, Garrigues V, Pertejo V, et al. Individual prediction of response to pneumatic dilation in patients with achalasia. Dig Dis Sci. 1996;41:2135-2141.Richards WO, Torquati A, Holzman MD, et al. Heller myotomy versus Heller myotomy with Dor fundoplication for acha-lasia: a prospective randomized double-blind clinical trial. Ann Surg. 2004;240(3):405-412; discussion 412-415.Shoenut J, Duerksen D. A prospective assessment of gastroesoph-ageal reflux before and after treatment of achalasia patients: pneumatic dilation versus transthoracic limited myotomy. Am J Gastroenterol. 1997;92:1109-1112.Spechler S, Castell DO. Classification of oesophageal motility abnormalities. Gut. 2001;49:145-151.Streitz JM, Jr, Glick ME, Ellis FH, Jr. Selective use of myotomy for treatment of epiphrenic diverticula: manometric and clinical analysis. Arch Surg. 1992;127:585-588.Vaezi MF, Baker ME, Achkar E, et al. Timed barium oesophogram: better predictor of long term success after | Surgery_Schwartz. 1995;130:632-636.Ponce J, Garrigues V, Pertejo V, et al. Individual prediction of response to pneumatic dilation in patients with achalasia. Dig Dis Sci. 1996;41:2135-2141.Richards WO, Torquati A, Holzman MD, et al. Heller myotomy versus Heller myotomy with Dor fundoplication for acha-lasia: a prospective randomized double-blind clinical trial. Ann Surg. 2004;240(3):405-412; discussion 412-415.Shoenut J, Duerksen D. A prospective assessment of gastroesoph-ageal reflux before and after treatment of achalasia patients: pneumatic dilation versus transthoracic limited myotomy. Am J Gastroenterol. 1997;92:1109-1112.Spechler S, Castell DO. Classification of oesophageal motility abnormalities. Gut. 2001;49:145-151.Streitz JM, Jr, Glick ME, Ellis FH, Jr. Selective use of myotomy for treatment of epiphrenic diverticula: manometric and clinical analysis. Arch Surg. 1992;127:585-588.Vaezi MF, Baker ME, Achkar E, et al. Timed barium oesophogram: better predictor of long term success after |
Surgery_Schwartz_7291 | Surgery_Schwartz | of epiphrenic diverticula: manometric and clinical analysis. Arch Surg. 1992;127:585-588.Vaezi MF, Baker ME, Achkar E, et al. Timed barium oesophogram: better predictor of long term success after pneumatic dilation in achalasia than symptom assessment. Gut. 2002;50:765-770.Verne G, Sallustio JE, Eaker EY. Anti-myenteric neuronal antibod-ies in patients with achalasia: a prospective study. Dig Dis Sci. 1997;42:307-313.Williams RB, Grehan MJ, Andre J, et al. Biomechanics, diagnosis, and treatment outcome in inflammatory myopathy presenting as oropharyngeal dysphagia. Gut. 2003;52:471-478.Zaninotto G, Annese V, Costantini M, et al. Randomized controlled trial of botulinum toxin versus laparoscopic Heller myotomy for esophageal achalasia. Ann Surg. 2004;239:364-370.Zhao X, Pasricha PJ. Botulinum toxin for spastic GI disorders: a systematic review. Gastrointest Endosc. 2003;57:219-235.Carcinoma of the EsophagusAkiyama H. Surgery for carcinoma of the esophagus. Curr Probl Surg. | Surgery_Schwartz. of epiphrenic diverticula: manometric and clinical analysis. Arch Surg. 1992;127:585-588.Vaezi MF, Baker ME, Achkar E, et al. Timed barium oesophogram: better predictor of long term success after pneumatic dilation in achalasia than symptom assessment. Gut. 2002;50:765-770.Verne G, Sallustio JE, Eaker EY. Anti-myenteric neuronal antibod-ies in patients with achalasia: a prospective study. Dig Dis Sci. 1997;42:307-313.Williams RB, Grehan MJ, Andre J, et al. Biomechanics, diagnosis, and treatment outcome in inflammatory myopathy presenting as oropharyngeal dysphagia. Gut. 2003;52:471-478.Zaninotto G, Annese V, Costantini M, et al. Randomized controlled trial of botulinum toxin versus laparoscopic Heller myotomy for esophageal achalasia. Ann Surg. 2004;239:364-370.Zhao X, Pasricha PJ. Botulinum toxin for spastic GI disorders: a systematic review. Gastrointest Endosc. 2003;57:219-235.Carcinoma of the EsophagusAkiyama H. Surgery for carcinoma of the esophagus. Curr Probl Surg. |
Surgery_Schwartz_7292 | Surgery_Schwartz | PJ. Botulinum toxin for spastic GI disorders: a systematic review. Gastrointest Endosc. 2003;57:219-235.Carcinoma of the EsophagusAkiyama H. Surgery for carcinoma of the esophagus. Curr Probl Surg. 1980;17:53-120.Akiyama H, Tsurumaru M. Radical lymph node dissection for cancer of the thoracic esophagus. Ann Surg. 1994;220(3):364-372.Altorki N, Skinner D. Should en-bloc esophagectomy be the standard of care for esophageal carcinoma? Ann Surg. 2001;234:581-587.Badwe RA, Sharma V, Bhansali MS, et al. The quality of swallow-ing for patients with operable esophageal carcinoma: a ran-domized trial comparing surgery with radiotherapy. Cancer. 1999;85:763-768.Baker JW, Jr, Schechter GL. Management of paraesophageal cancer by blunt resection without thoracotomy and reconstruction with stomach. Ann Surg. 1986;203:491-499.Brunicardi_Ch25_p1009-p1098.indd 109501/03/19 6:06 PM 1096SPECIFIC CONSIDERATIONSPART IIBiere SS, van Berge Henegouwen MI, Maas KW, et al. Minimally invasive open | Surgery_Schwartz. PJ. Botulinum toxin for spastic GI disorders: a systematic review. Gastrointest Endosc. 2003;57:219-235.Carcinoma of the EsophagusAkiyama H. Surgery for carcinoma of the esophagus. Curr Probl Surg. 1980;17:53-120.Akiyama H, Tsurumaru M. Radical lymph node dissection for cancer of the thoracic esophagus. Ann Surg. 1994;220(3):364-372.Altorki N, Skinner D. Should en-bloc esophagectomy be the standard of care for esophageal carcinoma? Ann Surg. 2001;234:581-587.Badwe RA, Sharma V, Bhansali MS, et al. The quality of swallow-ing for patients with operable esophageal carcinoma: a ran-domized trial comparing surgery with radiotherapy. Cancer. 1999;85:763-768.Baker JW, Jr, Schechter GL. Management of paraesophageal cancer by blunt resection without thoracotomy and reconstruction with stomach. Ann Surg. 1986;203:491-499.Brunicardi_Ch25_p1009-p1098.indd 109501/03/19 6:06 PM 1096SPECIFIC CONSIDERATIONSPART IIBiere SS, van Berge Henegouwen MI, Maas KW, et al. Minimally invasive open |
Surgery_Schwartz_7293 | Surgery_Schwartz | Ann Surg. 1986;203:491-499.Brunicardi_Ch25_p1009-p1098.indd 109501/03/19 6:06 PM 1096SPECIFIC CONSIDERATIONSPART IIBiere SS, van Berge Henegouwen MI, Maas KW, et al. Minimally invasive open oesophagectomy for patient with oesophageal cancer: a multicenter, open-label, randomized controlled trial. Lancet. 2012;19:1887-1892.Blazeby JM, Williams MH, et al. Quality of life measurement in patients with oesophageal cancer. Gut. 1995;37:505-508.Borrie J. Sarcoma of esophagus: surgical treatment. J Thorac Surg. 1959;37:413-426.Cameron AJ, Ott BJ, Payne WS. The incidence of adenocarci-noma in columnar-lined (Barrett’s) esophagus. N Engl J Med. 1985;313:857-859.Chang AC, Ji H, Birkmeyer NJ, et al. Outcomes after transhiatal and transthoracic esophagectomy for cancer. Ann Thorac Surg. 2008;85:424-429.Chang EY, Morris CD, Seltman AK, et al. The effect of antireflux surgery on esophageal carcinogenesis in patients with Barrett’s esophagus: a systematic review. Ann Surg. 2007;246:11-21.Clark | Surgery_Schwartz. Ann Surg. 1986;203:491-499.Brunicardi_Ch25_p1009-p1098.indd 109501/03/19 6:06 PM 1096SPECIFIC CONSIDERATIONSPART IIBiere SS, van Berge Henegouwen MI, Maas KW, et al. Minimally invasive open oesophagectomy for patient with oesophageal cancer: a multicenter, open-label, randomized controlled trial. Lancet. 2012;19:1887-1892.Blazeby JM, Williams MH, et al. Quality of life measurement in patients with oesophageal cancer. Gut. 1995;37:505-508.Borrie J. Sarcoma of esophagus: surgical treatment. J Thorac Surg. 1959;37:413-426.Cameron AJ, Ott BJ, Payne WS. The incidence of adenocarci-noma in columnar-lined (Barrett’s) esophagus. N Engl J Med. 1985;313:857-859.Chang AC, Ji H, Birkmeyer NJ, et al. Outcomes after transhiatal and transthoracic esophagectomy for cancer. Ann Thorac Surg. 2008;85:424-429.Chang EY, Morris CD, Seltman AK, et al. The effect of antireflux surgery on esophageal carcinogenesis in patients with Barrett’s esophagus: a systematic review. Ann Surg. 2007;246:11-21.Clark |
Surgery_Schwartz_7294 | Surgery_Schwartz | EY, Morris CD, Seltman AK, et al. The effect of antireflux surgery on esophageal carcinogenesis in patients with Barrett’s esophagus: a systematic review. Ann Surg. 2007;246:11-21.Clark GWB, Peters JH, Hagen JA, et al. Nodal metastases and recurrence patterns after en-bloc esophagectomy for adenocar-cinoma. Ann Thorac Surg. 1994;58:646-654.Clark GW, Smyrk TC, Burdiles P, et al. Is Barrett’s metapla-sia the source of adenocarcinomas of the cardia? Arch Surg. 1994;129:609-614.Collin CF, Spiro RH. Carcinoma of the cervical esophagus: chang-ing therapeutic trends. Am J Surg. 1984;148:460-466.Corley DA, Kerlikowske K, Verma R, et al. Protective association of aspirin/NSAIDs and esophageal cancer: a systematic review and meta-analysis. Gastroenterology. 2003;124:47-56.Cunningham D, Allum WH, Stenning SP, et al. Perioperative chemotherapy versus surgery alone for resectable gastro-esophageal cancer. N Engl J Med. 2006;6;355(1):11-20.Dallal HJ, Smith GD, Grieve DC, et al. A randomized trial | Surgery_Schwartz. EY, Morris CD, Seltman AK, et al. The effect of antireflux surgery on esophageal carcinogenesis in patients with Barrett’s esophagus: a systematic review. Ann Surg. 2007;246:11-21.Clark GWB, Peters JH, Hagen JA, et al. Nodal metastases and recurrence patterns after en-bloc esophagectomy for adenocar-cinoma. Ann Thorac Surg. 1994;58:646-654.Clark GW, Smyrk TC, Burdiles P, et al. Is Barrett’s metapla-sia the source of adenocarcinomas of the cardia? Arch Surg. 1994;129:609-614.Collin CF, Spiro RH. Carcinoma of the cervical esophagus: chang-ing therapeutic trends. Am J Surg. 1984;148:460-466.Corley DA, Kerlikowske K, Verma R, et al. Protective association of aspirin/NSAIDs and esophageal cancer: a systematic review and meta-analysis. Gastroenterology. 2003;124:47-56.Cunningham D, Allum WH, Stenning SP, et al. Perioperative chemotherapy versus surgery alone for resectable gastro-esophageal cancer. N Engl J Med. 2006;6;355(1):11-20.Dallal HJ, Smith GD, Grieve DC, et al. A randomized trial |
Surgery_Schwartz_7295 | Surgery_Schwartz | SP, et al. Perioperative chemotherapy versus surgery alone for resectable gastro-esophageal cancer. N Engl J Med. 2006;6;355(1):11-20.Dallal HJ, Smith GD, Grieve DC, et al. A randomized trial of thermal ablative therapy versus expandable metal stents in the palliative treatment of patients with esophageal carcinoma. Gastrointest Endosc. 2001;54:549-557.DeMeester TR, Skinner DB. Polypoid sarcomas of the esophagus. Ann Thorac Surg. 1975;20:405-417.Duhaylongsod FG, Wolfe WG. Barrett’s esophagus and adenocarci-noma of the esophagus and gastroesophageal junction. J Thorac Cardiovasc Surg. 1991;102:36-42.Ell C, May A, Gossner L, et al. Endoscopic mucosal resection of early cancer and high grade dysplasia in Barrett’s esophagus. Gastroenterology. 2001;118:670-677.Ellis FH, Heatley GJ, Krosna MJ, et al. Esophagogastrectomy for carcinoma of the esophagus and cardia: a comparison of find-ings and results after standard resection in three consecutive 8 year time intervals, using improved staging | Surgery_Schwartz. SP, et al. Perioperative chemotherapy versus surgery alone for resectable gastro-esophageal cancer. N Engl J Med. 2006;6;355(1):11-20.Dallal HJ, Smith GD, Grieve DC, et al. A randomized trial of thermal ablative therapy versus expandable metal stents in the palliative treatment of patients with esophageal carcinoma. Gastrointest Endosc. 2001;54:549-557.DeMeester TR, Skinner DB. Polypoid sarcomas of the esophagus. Ann Thorac Surg. 1975;20:405-417.Duhaylongsod FG, Wolfe WG. Barrett’s esophagus and adenocarci-noma of the esophagus and gastroesophageal junction. J Thorac Cardiovasc Surg. 1991;102:36-42.Ell C, May A, Gossner L, et al. Endoscopic mucosal resection of early cancer and high grade dysplasia in Barrett’s esophagus. Gastroenterology. 2001;118:670-677.Ellis FH, Heatley GJ, Krosna MJ, et al. Esophagogastrectomy for carcinoma of the esophagus and cardia: a comparison of find-ings and results after standard resection in three consecutive 8 year time intervals, using improved staging |
Surgery_Schwartz_7296 | Surgery_Schwartz | et al. Esophagogastrectomy for carcinoma of the esophagus and cardia: a comparison of find-ings and results after standard resection in three consecutive 8 year time intervals, using improved staging criteria. J Thorac Cardiovasc Surg. 1997;113:836.Frenken M. Best palliation in esophageal cancer; surgery, stenting, radiation, or what? Dis Esophagus. 2001;14:120-123.Fujita H, Kakegawa T, Yamana H, et al. Mortality and morbidity rates, postoperative course, quality of life, and prognosis after extended radical lymphadenectomy for esophageal cancer. Ann Surg. 1995;222:654-662.Gebski V, Burmeister B, Smithers BM, et al. Survival benefits from neoadjuvant chemoradiotherapy or chemotherapy in oesophageal carcinoma: a meta-analysis. Lancet. 2007;8(3): 226-234.Greenstein AJ, Litle VR, Swanson SJ, et al. Effect of the num-ber of lymph nodes sampled on postoperative survival of lymph node-negative esophageal cancer. Cancer. 2008;112: 1239-1246.Hagen JA, DeMeester SR, Peters JH, Chandrasoma P, | Surgery_Schwartz. et al. Esophagogastrectomy for carcinoma of the esophagus and cardia: a comparison of find-ings and results after standard resection in three consecutive 8 year time intervals, using improved staging criteria. J Thorac Cardiovasc Surg. 1997;113:836.Frenken M. Best palliation in esophageal cancer; surgery, stenting, radiation, or what? Dis Esophagus. 2001;14:120-123.Fujita H, Kakegawa T, Yamana H, et al. Mortality and morbidity rates, postoperative course, quality of life, and prognosis after extended radical lymphadenectomy for esophageal cancer. Ann Surg. 1995;222:654-662.Gebski V, Burmeister B, Smithers BM, et al. Survival benefits from neoadjuvant chemoradiotherapy or chemotherapy in oesophageal carcinoma: a meta-analysis. Lancet. 2007;8(3): 226-234.Greenstein AJ, Litle VR, Swanson SJ, et al. Effect of the num-ber of lymph nodes sampled on postoperative survival of lymph node-negative esophageal cancer. Cancer. 2008;112: 1239-1246.Hagen JA, DeMeester SR, Peters JH, Chandrasoma P, |
Surgery_Schwartz_7297 | Surgery_Schwartz | et al. Effect of the num-ber of lymph nodes sampled on postoperative survival of lymph node-negative esophageal cancer. Cancer. 2008;112: 1239-1246.Hagen JA, DeMeester SR, Peters JH, Chandrasoma P, DeMeester TR. Curative resection for esophageal adenocarcinoma analy-sis of 100 en bloc esophagectomies. Ann Surg. 2001;234(4): 520-531.Hofstetter W, Swisher SG, Correa AM, et al. Treatment outcomes of resected esophageal cancer. Ann Surg. 2002;236:376-385.Hulscher JB, Van Sandick JW, de Boer AG, et al. Extended transthoracic resection compared with limited transhiatal resection for adenocarcinoma of the esophagus. N Engl J Med. 2002;347(21):1662-1669.Iijima K, Henrey E, Moriya A, et al. Dietary nitrate generates poten-tially mutagenic concentrations of nitric oxide at the gastro-esophageal junction. Gastroenterology. 2002;122:1248-1257.Ikeda M, Natsugoe S, Ueno S, et al. Significant host and tumor related factors for predicting prognosis in patients with esopha-geal carcinoma. Ann Surg. | Surgery_Schwartz. et al. Effect of the num-ber of lymph nodes sampled on postoperative survival of lymph node-negative esophageal cancer. Cancer. 2008;112: 1239-1246.Hagen JA, DeMeester SR, Peters JH, Chandrasoma P, DeMeester TR. Curative resection for esophageal adenocarcinoma analy-sis of 100 en bloc esophagectomies. Ann Surg. 2001;234(4): 520-531.Hofstetter W, Swisher SG, Correa AM, et al. Treatment outcomes of resected esophageal cancer. Ann Surg. 2002;236:376-385.Hulscher JB, Van Sandick JW, de Boer AG, et al. Extended transthoracic resection compared with limited transhiatal resection for adenocarcinoma of the esophagus. N Engl J Med. 2002;347(21):1662-1669.Iijima K, Henrey E, Moriya A, et al. Dietary nitrate generates poten-tially mutagenic concentrations of nitric oxide at the gastro-esophageal junction. Gastroenterology. 2002;122:1248-1257.Ikeda M, Natsugoe S, Ueno S, et al. Significant host and tumor related factors for predicting prognosis in patients with esopha-geal carcinoma. Ann Surg. |
Surgery_Schwartz_7298 | Surgery_Schwartz | Gastroenterology. 2002;122:1248-1257.Ikeda M, Natsugoe S, Ueno S, et al. Significant host and tumor related factors for predicting prognosis in patients with esopha-geal carcinoma. Ann Surg. 2003;238:197-202.Jankowski JA, Wight NA, Meltzer SJ, et al. Molecular evolution of the metaplasia-dysplasia-adenocarcinoma sequence in the esophagus. Am J Pathol. 1999;154:965-973.Jobe BA, Kim CY, Minjarez RC, et al. Simplifying minimally invasive transhiatal esophagectomy with the inversion approach: lessons learned from the first 20 cases. Arch Surg. 2006;141:857-865; discussion 865.Johansson J, DeMeester TR, Hoger JA, et al. En bloc is supe-rior to transhiatal esophagectomy for T3 N1 adenocarci-noma of the distal esophagus and GE junction. Arch Surg. 2004;139:627-633.Kaklamanos IG, Walker GR, Ferry K, et al. Neoadjuvant treatment for resectable cancer of the esophagus and the gastroesophageal junction: a meta-analysis of randomized clinical trials. Ann Surg Oncol. 2003;10:754-761.Kelsen DP, | Surgery_Schwartz. Gastroenterology. 2002;122:1248-1257.Ikeda M, Natsugoe S, Ueno S, et al. Significant host and tumor related factors for predicting prognosis in patients with esopha-geal carcinoma. Ann Surg. 2003;238:197-202.Jankowski JA, Wight NA, Meltzer SJ, et al. Molecular evolution of the metaplasia-dysplasia-adenocarcinoma sequence in the esophagus. Am J Pathol. 1999;154:965-973.Jobe BA, Kim CY, Minjarez RC, et al. Simplifying minimally invasive transhiatal esophagectomy with the inversion approach: lessons learned from the first 20 cases. Arch Surg. 2006;141:857-865; discussion 865.Johansson J, DeMeester TR, Hoger JA, et al. En bloc is supe-rior to transhiatal esophagectomy for T3 N1 adenocarci-noma of the distal esophagus and GE junction. Arch Surg. 2004;139:627-633.Kaklamanos IG, Walker GR, Ferry K, et al. Neoadjuvant treatment for resectable cancer of the esophagus and the gastroesophageal junction: a meta-analysis of randomized clinical trials. Ann Surg Oncol. 2003;10:754-761.Kelsen DP, |
Surgery_Schwartz_7299 | Surgery_Schwartz | K, et al. Neoadjuvant treatment for resectable cancer of the esophagus and the gastroesophageal junction: a meta-analysis of randomized clinical trials. Ann Surg Oncol. 2003;10:754-761.Kelsen DP, Winter KA, Gunderson LL, et al. Long-term results of RTOG trial 8911 (USA Intergroup 113): a random assign-ment trial comparison of chemotherapy followed by surgery compared with surgery alone for esophageal cancer. J Clin Oncol. 2007;25(24):3719-3725.Krasna MJ, Reed CE, Nedzwiecki D, et al. CALBG 9380: a prospec-tive trial of the feasibility of thoracoscopy/laparoscopy in stag-ing esophageal cancer. Ann Thorac Surg. 2001;71:1073-1079.Kirby JD. Quality of life after esophagectomy: the patients’ per-spective. Dis Esophagus. 1999;12:168-171.Lagergren J, Bergstrom R, Lindgren A, Nyrén O. Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med. 1999;340(11):825-831.Lavin P, Hajdu SI, Foote FW, Jr. Gastric and extragastric leiomyo-blastomas. Cancer. | Surgery_Schwartz. K, et al. Neoadjuvant treatment for resectable cancer of the esophagus and the gastroesophageal junction: a meta-analysis of randomized clinical trials. Ann Surg Oncol. 2003;10:754-761.Kelsen DP, Winter KA, Gunderson LL, et al. Long-term results of RTOG trial 8911 (USA Intergroup 113): a random assign-ment trial comparison of chemotherapy followed by surgery compared with surgery alone for esophageal cancer. J Clin Oncol. 2007;25(24):3719-3725.Krasna MJ, Reed CE, Nedzwiecki D, et al. CALBG 9380: a prospec-tive trial of the feasibility of thoracoscopy/laparoscopy in stag-ing esophageal cancer. Ann Thorac Surg. 2001;71:1073-1079.Kirby JD. Quality of life after esophagectomy: the patients’ per-spective. Dis Esophagus. 1999;12:168-171.Lagergren J, Bergstrom R, Lindgren A, Nyrén O. Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med. 1999;340(11):825-831.Lavin P, Hajdu SI, Foote FW, Jr. Gastric and extragastric leiomyo-blastomas. Cancer. |
Surgery_Schwartz_7300 | Surgery_Schwartz | gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med. 1999;340(11):825-831.Lavin P, Hajdu SI, Foote FW, Jr. Gastric and extragastric leiomyo-blastomas. Cancer. 1972;29:305-311.Law SYK, Fok M, Wong J. Pattern of recurrence after oesopha-geal resection for cancer: clinical implications. Br J Surg. 1996;83(1):107-111.Law SYK, Fok M, et al. A comparison of outcomes after resec-tion for squamous cell carcinomas and adenocarcinomas of the esophagus and cardia. Surg Gynecol Obstet. 1992;175:107-112.Law S, Kwong DL, Kwok KF, et al. Improvement in treatment results and long term survival of patients with esophageal cancer: impact of chemoradiation and change in treatment strategy. Ann Surg. 2003;238:339-347.Lerut T, Coosemans W, Van Raemdonck D, et al. Surgical treat-ment of Barrett’s carcinoma. Correlations between morpho-logic findings and prognosis. J Thorac Cardiovasc Surg. 1994;107:1059-1066.Leuketich JD, Alvelo-Rivera M, Buenaventura PO, et al. Mini-mally | Surgery_Schwartz. gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med. 1999;340(11):825-831.Lavin P, Hajdu SI, Foote FW, Jr. Gastric and extragastric leiomyo-blastomas. Cancer. 1972;29:305-311.Law SYK, Fok M, Wong J. Pattern of recurrence after oesopha-geal resection for cancer: clinical implications. Br J Surg. 1996;83(1):107-111.Law SYK, Fok M, et al. A comparison of outcomes after resec-tion for squamous cell carcinomas and adenocarcinomas of the esophagus and cardia. Surg Gynecol Obstet. 1992;175:107-112.Law S, Kwong DL, Kwok KF, et al. Improvement in treatment results and long term survival of patients with esophageal cancer: impact of chemoradiation and change in treatment strategy. Ann Surg. 2003;238:339-347.Lerut T, Coosemans W, Van Raemdonck D, et al. Surgical treat-ment of Barrett’s carcinoma. Correlations between morpho-logic findings and prognosis. J Thorac Cardiovasc Surg. 1994;107:1059-1066.Leuketich JD, Alvelo-Rivera M, Buenaventura PO, et al. Mini-mally |
Surgery_Schwartz_7301 | Surgery_Schwartz | of Barrett’s carcinoma. Correlations between morpho-logic findings and prognosis. J Thorac Cardiovasc Surg. 1994;107:1059-1066.Leuketich JD, Alvelo-Rivera M, Buenaventura PO, et al. Mini-mally invasive esophagectomy: outcomes in 222 patients. Ann Surg. 2003;238(4):486-494.Levine DS, Reid BJ. Endoscopic diagnosis of esophageal neo-plasms. Gastrointest Clin North Am. 1992;2:395-413.Lewis I. The surgical treatment of carcinoma of the esophagus with special reference to a new operation for the growths of the mid-dle third. Br J Surg. 1946;34:18-31.Logan A. The surgical treatment of carcinoma of the esophagus and cardia. J Thorac Cardiovasc Surg. 1963;46:150-161.Manner H, May A, Pech O, et al. Early Barrett’s carcinoma with “low-risk” submucosal invasion: long-term results of endo-scopic resection with a curative intent. Am J Gastroenterol. 2008;103:2589-2597.Brunicardi_Ch25_p1009-p1098.indd 109601/03/19 6:06 PM 1097ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25McCort JJ. Esophageal | Surgery_Schwartz. of Barrett’s carcinoma. Correlations between morpho-logic findings and prognosis. J Thorac Cardiovasc Surg. 1994;107:1059-1066.Leuketich JD, Alvelo-Rivera M, Buenaventura PO, et al. Mini-mally invasive esophagectomy: outcomes in 222 patients. Ann Surg. 2003;238(4):486-494.Levine DS, Reid BJ. Endoscopic diagnosis of esophageal neo-plasms. Gastrointest Clin North Am. 1992;2:395-413.Lewis I. The surgical treatment of carcinoma of the esophagus with special reference to a new operation for the growths of the mid-dle third. Br J Surg. 1946;34:18-31.Logan A. The surgical treatment of carcinoma of the esophagus and cardia. J Thorac Cardiovasc Surg. 1963;46:150-161.Manner H, May A, Pech O, et al. Early Barrett’s carcinoma with “low-risk” submucosal invasion: long-term results of endo-scopic resection with a curative intent. Am J Gastroenterol. 2008;103:2589-2597.Brunicardi_Ch25_p1009-p1098.indd 109601/03/19 6:06 PM 1097ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25McCort JJ. Esophageal |
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