Search

Attention has been focused on the amplitude of esophageal body contraction to avoid persistent dysphagia after a Nissen fundoplication. The current recommended level is a contraction amplitude in the distal third of esophagus above the fifth percentile. We hypothesized that a more physiologic approach is to measure outflow resistance imposed by a fundoplication, which needs to be overcome by the esophageal contraction amplitude.The esophageal outflow resistance, as reflected by the intra-bolus pressure (iBP) measured 5 cm above the lower esophageal sphincter (LES), was measured in 53 normal subjects and 37 reflux patients with normal esophageal contraction amplitude, before and after a standardized Nissen fundoplication. All were free of postoperative dysphagia. A test population of 100 patients who had a Nissen fundoplication was used to validate the threshold of outflow resistance to avoid persistent postoperative dysphagia.The mean (SD) amplitude of the iBP in normal subjects was 6.8 (3.7) mmHg and in patients before fundoplication was 3.6 (7.0) mmHg (p = 0.003). After Nissen fundoplication, the mean (SD) amplitude of the iBP increased to 12.0 (3.2) mmHg (p0.0001 vs normal subjects or preoperative values). The 95th percentile value for iBP after a Nissen fundoplication was 20.0 mmHg and was exceeded by esophageal contraction in all patients in the validation population, and 97% of these patients were free of persistent postoperative dysphagia at a median 50-month follow-up.Nissen fundoplication increases the outflow resistance of the esophagus and should be constructed to avoid an iBP20 mmHg. Patients whose distal third esophageal contraction amplitude is20 mmHg have a minimal risk of dysphagia after a tension-free Nissen fundoplication.

Patients with respiratory and laryngeal symptoms are commonly referred for evaluation of reflux disease as a potential cause. Dual-probe pH monitoring is often performed, although data on normal acid exposure in the proximal esophagus are limited because of the small number of normal subjects and inconsistent placement of the proximal pH sensor in relation to the upper esophageal sphincter. We measured proximal esophageal acid exposure using dual-probe pH and calculated a composite pH score in a large number of asymptomatic volunteers to better define normal values.Eighty-one normal subjects free of reflux, laryngeal, or respiratory symptoms were recruited. All had video esophagraphy to exclude hiatal hernia. Esophageal pH monitoring was performed using 1 of 3 different dual-probe catheters with sensors spaced 10, 15, or 18 cm apart. The standard components of esophageal acid exposure were measured, excluding meal periods. A composite pH score for the proximal esophagus was calculated using these components.The final study population consisted of 59 (49% male) subjects, with a median age of 27 years. All had normal distal esophageal acid exposure and no hiatal hernia. The 95(th) percentile values for the percent time the pH was4 for the total, upright, and supine periods were 0.9%, 1.2%, and 0.4%, respectively. The 95(th) percentile for the number of reflux episodes was 24 and for the calculated proximal esophageal composite pH score was 16.4.In a large population of normal subjects, we have defined the normal values and calculated a composite pH score for proximal esophageal acid exposure. The total percent time pH4 was similar to previously published normal values, but the number of reflux episodes was greater.

Background Ischemia of the gastric conduit remains an important complication of esophagectomy and is associated with an increased risk of anastomotic leak and sepsis. We report a group of patients with multiple comorbid conditions and an ischemic gastric conduit that was successfully managed by a delayed esophagogastrostomy. Study Design Between 2000 and 2007, esophagectomy with gastric pullup was performed in 554 patients. In 37 patients (7%), the combination of an ischemic graft and substantial comorbid conditions prompted delayed reconstruction to avoid an immediate esophagogastrostomy. In these patients, the gastric conduit was brought up and secured in the neck, and a cervical esophagostomy was constructed. Subsequently, a delayed esophagogastrostomy was performed through neck incision. Outcomes were analyzed at a median of 22 months (interquartile range [IQR], 13 to 30 months). Results There were 29 male and 8 female patients, with a median age of 65 years (IQR, 58 to 75 years). Thirty-one patients had malignant disease; 12 received neoadjuvant therapy. All 37 patients recovered from their esophagectomy without evidence of ischemic necrosis or fistula from their gastric conduit. In 35 patients, a delayed esophagogastrostomy was performed at a median of 98 days (IQR, 89 to 110 days). At the time of reconstruction, all had well-perfused gastric conduits, and the anastomoses healed without leak, wound infection, or sepsis. A stricture developed in three patients and was treated with dilation. Delayed esophagogastrostomy was never performed in two patients because of development of recurrent malignant disease. Conclusions Delayed esophagogastrostomy is a safe strategy for management of patients with comorbidities and an ischemic gastric conduit at the time of esophagectomy.

Background Mucosal ablation and endoscopic mucosal resection have been proposed as alternatives to surgical resection as therapy for intramucosal adenocarcinoma (IMC) of the esophagus. Acceptance of these alternative therapies requires an understanding of the clinical biology of IMC and the results of surgical resection modified for treatment of early disease. Study design Retrospective review of 78 patients (65 men, 13 women; median age 66 years) with IMC who were treated with progressively less-extensive surgical resections (ie, en bloc, transhiatal, and vagal-sparing esophagectomy) from 1987 to 2005. Results The tumor was located in a visible segment of Barrett's esophagus in 65 (83%) and in cardia intestinal metaplasia in 13 (17%). A visible lesion was present in 53 (68%) and in all but 4 the lesion was cancer. In those patients with visible Barrett's, the tumor was within 3 cm of the gastroesophageal junction in 66% and within 1 cm in 37%. Esophagectomy was en bloc in 23, transhiatal in 31, vagal-sparing in 20, and transthoracic in 4. Operative mortality was 2.6%. Vagal-sparing esophagectomy had less morbidity, a shorter hospital stay, and no mortality. Of the patients who had en bloc resection, a median of 41 nodes were removed. One patient had one lymph node metastasis on hematoxylin and eosin staining and two others, normal on hematoxylin and eosin staining, had micrometastases on immunohistochemistry. Actuarial survival at 5 years was 88% and was similar for all types of resections. Two patients died from systemic metastases and seven from noncancer causes. Conclusions IMC occurred in cardia intestinal metaplasia and in Barrett's esophagus. Two-thirds of patients with IMC had a visible lesion. Most tumors occurred near the gastroesophageal junction. Node metastases were uncommon, questioning the need for lymphadenectomy. A vagal-sparing technique had less morbidity than other forms of resection and no mortality. Survival after all types of resection was similar. Outcomes of endoscopic techniques should be compared with this benchmark.

Background Surgery, as the mainstay of treatment for localized esophageal cancer, is currently being challenged by the assumed high risk of esophagectomy and the poor longterm survival after resection. Epidemiologic and clinical changes over the past decade indicate that these assumptions should be reevaluated. The aim of this study was to assess the modern outcomes of esophagectomy for adenocarcinoma. Study design We studied 263 consecutive patients (215 men, 48 women), who had esophagectomy for adenocarcinoma from 1992 to 2002. Ninety-seven (37%) were stage I, 63 (24%) were stage II, 93 (35%) were stage III, and 10 (4%) were stage IV. Forty-five percent (119 of 263) had curative en bloc resection, 52% (138 of 263) had node involvement, and 18% (48) received neoadjuvant therapy. Results Seventeen percent (44 of 263) of the patients were identified in a Barrett's surveillance program. The frequency of T1N0 adenocarcinoma increased over the study period (p=0.024). The overall 5-year survival was 46.5%, and for the last 5 years of the study was 50.4%. The overall 5-year survival for stage I was 81%; for stage II, 51%; for stage III, 14%; and for stage IV, 0%. Complications occurred in 61% and there were 12 perioperative deaths (4.5%). Cox proportional hazard analysis identified tumor stage and type of resection as independent predictors of survival. Conclusions Nearly half of patients undergoing esophagectomy for adenocarcinoma survive ≥5 years. Improvements in survival are associated with increased detection of early stage disease, and a liberal use of en bloc resection. Nonsurgical treatments should be compared with these contemporary outcomes measures.

Background Reports of esophageal anastomotic complications often involve more gastric than colonic reconstructions and are incomplete because of fragmented followup by physicians unfamiliar with the surgical procedure. Study design Three hundred ninety-three consecutive esophagectomy patients had prevalence and risk factors determined for graft ischemia and anastomotic leak; 363 of these patients followed for more than 1 month (median 15 months) had prevalence and risk factors determined for anastomotic stricture. Results Conduit ischemia occurred in 36 (9.2%) and anastomotic leak in 43 patients (10.9%). Risk factor for ischemia was comorbid conditions requiring therapy (Odds ratio [OR]: 2.2 [95% CI 1.1–4.3]), and for leak were ischemia (OR: 5.5 [95% CI 2.5–12.1]), neoadjuvant therapy (OR: 2.2 [95% CI 1.1–4.5]), and comorbid conditions (OR: 2.1 [95% CI 1.1–3.9]). A stricture developed in 80 patients (22.0%). Risk factors were ischemia (OR: 4.4 [95% CI 2.0–9.6]), anastomotic leak (OR: 3.8 [95% CI 1.9–7.6]), and increasing preoperative weight (p = 0.022). The prevalence of ischemia was similar after gastric (10.4%) versus colonic (7.4%) reconstruction; leak and stricture were more common (14.3% versus 6.1%, p=0.013, 31.3% versus 8.7%, p Conclusions After esophagectomy 10% of patients will develop conduit ischemia or an anastomotic leak and 22% will develop anastomotic stricture. Anastomotic leak and strictures are more common and the strictures are more severe after gastric pull-up compared with colon interposition. Dilatation is a safe and effective treatment.

Background: Recent studies based on symptomatic outcomes analyses have shown that laparoscopic repair of large type III hiatal hernias is safe, successful, and equivalent to open repair. These outcomes analyses were based on a relatively short followup period and lack objective confirmation that the hernia has not recurred. The aim of this study was to compare the outcomes of laparoscopic and open repair of large type III hiatal hernia using both symptomatic evaluation and barium study to assess the integrity of the repair. Study Design: Fifty-four patients underwent repair of a large type III hiatal hernia between 1985 and 1998. The surgical approach was laparotomy in 13, thoracotomy in 14, and laparoscopy in 27. An antireflux procedure was included in all patients. Symptomatic outcomes were assessed using a structured questionnaire at a median of 24 months and was complete in 51 of 54 patients (94%). A single radiologist, without knowledge of the operative procedure, assessed the integrity of the repair using video esophagram. Videos were performed at a median of 27 months (35 months open and 17 laparoscopic) and were completed in 41 of 54 patients (75%). Results: Symptomatic outcomes were similar in both groups with excellent or good outcomes in 76% of the patients after laparoscopic repair and 88% after an open repair. Reherniation was present in 12 patients and was asymptomatic in 7. A recurrent hernia was present in 12 of the 41 patients (29%) who returned for a followup video esophagram. Forty-two percent (9 of 21) of the laparoscopic group had a recurrent hernia compared with 15% (3 of 20) of the open group (p Conclusions: Laparoscopic repair of type III hiatal hernias is associated with a disturbingly high (42%) prevalence of recurrent hernia. More than half such recurrences have few, if any, symptoms.

Background To determine the optimal follow-up strategy after esophagectomy for adenocarcinoma of the esophagus or gastroesophageal junction by evaluating the timing of recurrence and the method that first detected the recurrence. Study Design Between 1991 and 2007, 590 patients had an esophagectomy for adenocarcinoma. Recurrence occurred in 233 (40%) and, of those, 174 had complete follow-up at our center with a protocol that consisted of an office visit with CT scans and laboratory studies every 3 months for 3 years, every 6 months for 2 years, and then annually. A subset of patients had PET annually. Results Recurrence in the 174 patients with complete follow-up was systemic in 104 (60%), locoregional/nodal in 51 (30%), and both in 19 (10%). Recurrence was first suspected by symptoms and/or physical examination in 29 patients (17%), by CT scan in 105 (60%), PET in 32 (18%), and by elevated CEA in 8 (5%). Recurrence was detected at a median of 11 months (range 3 to 72 months) and occurred later after esophagectomy alone compared with patients who received neoadjuvant therapy (12 versus 8 months; p=0.01), but the pattern of recurrence was similar. More than 90% of recurrences were detected within 2 years after neoadjuvant therapy, compared with 3 years after esophagectomy alone. Median survival after recurrence was 7 months and was significantly longer in patients treated for the recurrence (9 versus 3 months; p=0.001). Conclusions Frequent early follow-up is appropriate after esophagectomy for adenocarcinoma because >90% of recurrences will occur by 3 years after esophagectomy alone and by 2 years following neoadjuvant therapy. Beyond these time periods, 2% to 3% of recurrences were detected each year, suggesting that annual follow-up is adequate. Survival after recurrence was improved with therapy, confirming the use of careful follow-up in these patients.

Background After esophagectomy, many patients who received neoadjuvant therapy have no evidence of lymph node involvement (N0 disease). Whether lymph nodes were initially involved and eradicated by the neoadjuvant therapy (down-staged) or if the nodes were never involved is a subject of debate. To address this issue, we compared clinical outcomes in N0 patients treated with neoadjuvant therapy with outcomes in patients treated with surgery alone. Study Design We reviewed records of 100 consecutive patients who underwent R0 esophagectomy for adenocarcinoma with pathologic N0 status. Seventy-five patients were treated by operation alone and 25 received neoadjuvant therapy. Tumor characteristics including length, depth, lymphovascular invasion, and degree of differentiation were compared and longterm survival was assessed by Kaplan-Meier analysis at a median of 46 months (interquartile range 26 to 77 months). Results Tumor characteristics were similar between groups. Recurrence was more common in patients who received neoadjuvant therapy compared with those treated with surgery alone (10 of 25 versus 10 of 75, p=0.0063). Patients with N0 disease after neoadjuvant therapy had a significantly worse survival than patients treated by surgery alone (49% versus 85%, p=0.005). Conclusions Although neoadjuvant therapy may eradicate lymph node metastases, it does not result in the same outcomes as those achieved in patients with N0 disease treated with surgery alone. The poor clinical outcomes observed in N0 patients after neoadjuvant therapy suggest that they initially had node involvement and were downstaged by eradication of lymph node disease.

Background Carcinoembryonic antigen (CEA) and plasma DNA are known to be elevated in patients with esophageal cancer and are higher in patients with disseminated disease. The sensitivity and specificity of these markers in the diagnosis of recurrent esophageal cancer have not been compared. Study Design Plasma DNA was measured using polymerase chain reaction in 45 patients with esophageal cancer and 44 asymptomatic volunteers. The 95 th percentile (19 ng /mL) in the volunteers was used to define normal. Thirty-nine patients had localized cancer and underwent resection, and six had disseminated disease at operation. Plasma DNA was measured preoperatively in all patients, with serum CEA measured in 31. Plasma DNA was measured sequentially during followup in 21 patients, including 7 who developed recurrence. CEA was measured in 14 of 21 patients who had sequential plasma DNA measured and in 6 of 7 patients with recurrence. CEA levels greater than 5.0 ng/mL were used as cut-off. Results Plasma DNA was more sensitive than CEA for detecting unresectable esophageal cancer (100% versus 40%), but it had a lower specificity (22% versus 89%).The positive predictive value (19% versus 40%) and negative predictive value (100% versus 89%) were similar for plasma DNA and serum CEA, respectively. Plasma DNA was also more sensitive than CEA in detecting recurrent esophageal cancer (100% versus 33%). The specificity and positive predictive values were 100% for both tests, but the negative predictive values were higher for plasma DNA. Plasma DNA rose before there was clinical evidence of recurrence in 67% compared with only 17% for CEA. Conclusions Elevated plasma DNA is an extremely reliable indicator of the presence of recurrent disease, and, in the majority of patients, it rises before clinical evidence of recurrence. In contrast, a normal CEA should be interpreted cautiously, because it does not exclude recurrent disease.

Reports of esophageal anastomotic complications often involve more gastric than colonic reconstructions and are incomplete because of fragmented followup by physicians unfamiliar with the surgical procedure.Three hundred ninety-three consecutive esophagectomy patients had prevalence and risk factors determined for graft ischemia and anastomotic leak; 363 of these patients followed for more than 1 month (median 15 months) had prevalence and risk factors determined for anastomotic stricture.Conduit ischemia occurred in 36 (9.2%) and anastomotic leak in 43 patients (10.9%). Risk factor for ischemia was comorbid conditions requiring therapy (Odds ratio [OR]: 2.2 [95% CI 1.1-4.3]), and for leak were ischemia (OR: 5.5 [95% CI 2.5-12.1]), neoadjuvant therapy (OR: 2.2 [95% CI 1.1-4.5]), and comorbid conditions (OR: 2.1 [95% CI 1.1-3.9]). A stricture developed in 80 patients (22.0%). Risk factors were ischemia (OR: 4.4 [95% CI 2.0-9.6]), anastomotic leak (OR: 3.8 [95% CI 1.9-7.6]), and increasing preoperative weight (p = 0.022). The prevalence of ischemia was similar after gastric (10.4%) versus colonic (7.4%) reconstruction; leak and stricture were more common (14.3% versus 6.1%, p = 0.013, 31.3% versus 8.7%, p0.0001, respectively) and strictures were more severe (11.2% versus 2%, p = 0.001) after gastric pull-up. Patients free of ischemia and leak who developed stricture were more likely to have had a gastric pull-up (25% versus 7%, p0.0001). Dilatation was effective treatment in 93% of patients.After esophagectomy 10% of patients will develop conduit ischemia or an anastomotic leak and 22% will develop anastomotic stricture. Anastomotic leak and strictures are more common and the strictures are more severe after gastric pull-up compared with colon interposition. Dilatation is a safe and effective treatment.

To investigate the factors leading to histologic regression of metaplastic and dysplastic Barrett's esophagus (BE).The study sample consisted of 91 consecutive patients with symptomatic Barrett's esophagus. Pre- and posttreatment endoscopic biopsies from 77 Barrett's patients treated surgically and 14 treated with proton pump inhibitors (PPI) were reviewed. An expert pathologist confirmed the presence of intestinal metaplasia (IM) with or without dysplasia. Posttreatment histology was classified as having regressed if two consecutive biopsies taken more than 6 months apart plus all subsequent biopsies showed loss of IM or loss of dysplasia. Clinical factors associated with regression were studied by multivariate analysis, as was the time course of its occurrence.Histopathologic regression occurred in 28 of 77 patients (36.4%) after antireflux surgery and in 1 of 14 patients (7.1%) treated with PPIs alone (p0.03). After surgery, regression from low-grade dysplastic to nondysplastic BE occurred in 17 of 25 patients (68%) and from IM to no IM in 11 of 52 (21.2%). Both types of regression were significantly more common in short (3 cm) than long (3 cm) segment Barrett's esophagus; 19 of 33 (58%) and 9 of 44 (20%) patients, respectively (p = 0.0016). Eight patients progressed, five from IM alone to low-grade dysplasia and three from low- to high-grade dysplasia. All those who progressed had long segment BE. On multivariate analysis, presence of short segment Barrett's and type of treatment were significantly associated with regression; age, gender, surgical procedure, and preoperative lower esophageal sphincter and pH characteristics were not. The median time of biopsy-proved regression was 18.5 months after surgery, with 95% occurring within 5 years.This study refutes the widely held assumption that once established, Barrett's esophagus does not change. More than one-third of patients with visible segments of Barrett's esophagus undergo histologic regression after antireflux surgery. Regression is dependent on the length of the columnar-lined esophagus and time of followup after antireflux surgery.