Reijiro Saito

Hand-Sewn Cervical Anastomosis Versus Stapled Intrathoracic Anastomosis After Esophagectomy for Middle or Lower Thoracic Esophageal Cancer: A Prospective Randomized Controlled Study

PurposeThe type of anastomosis and its outcome can affect postoperative morbidity, mortality, and quality of life after esophagectomy. We compared the outcomes of cervical hand-sewn anastomosis (CHS) and intrathoracic stapled anastomosis (ITS) performed after esophagectomy and gastric reconstruction.MethodsThirty-two patients with middle or lower thoracic esophageal cancer were prospectively randomized to undergo CHS (n = 18) or ITS (n = 14) after esophagectomy. We compared clinical data, postoperative symptoms, and long-term survival in the two groups.ResultsThe rates of anastomotic leak and stricture in the CHS and ITS groups were 16.7% versus 7.1% and 0% versus 14.2%, respectively, which do not represent significant differences. The respective rates of recurrent laryngeal nerve palsy were 38.8% versus 7.1% (P < 0.05), and proximal esophageal resection was 15 mm longer (P < 0.05) in the CHS group. There were no significant differences in symptoms 6 months after surgery, or in the overall 5-year survival rates (72.2% and 85.7%, respectively).ConclusionsThe two methods of anastomosis yielded similar anastomotic outcomes. Although the incidence of recurrent laryngeal nerve injury was higher after CHS, and proximal esophageal resection was longer, this had little impact on postoperative symptoms and long-term survival.

Analysis of results of surgery performed over a 20-year period on 500 patients with cancer of the thoracic esophagus

This study was conducted to examine the long-term outcome of 500 patients who underwent surgery for cancer of the thoracic esophagus during the past 20 years. Favorable results were obtained with postoperative adjuvant radiation and chemotherapy and there were no surgical deaths in the last 5 years. The mortality rate decreased from 17% prior to 1980 to 5% between 1981 and 1993, this being most probably attributable to the decreased incidence of suture leakage. With respect to changes in surgical techniques, during the initial years we performed intrathoracic anastomosis, after which sternal manubrium resection with anterior mediastinal esophagogastrostomy was carried out. Subsequently, we invented a technique for performing esophagogastrostomy via the posterior mediastinum. The posterior mediastinum was selected as the most physiologic route, based on measurement of tissue oxygen tension. Using blood flow determinations obtained by laser-Doppler velocimetry, we concluded that the effectiveness of thicker gastric tubes was superior to that of thin tubes. Esophagogastrostomy was performed in a shallow field in the cervical region, with the anastomosis ultimately positioned in the superior mediastinum and covered with mediastinal pleura.

Outcome and Treatment Strategy for Mid- and Lower-Thoracic Esophageal Cancer Recurring Locally in the Lymph Nodes of the Neck

The aim of the present study was to assess the outcome of treatment for patients with recurrent mid- and lower-thoracic esophageal cancers in whom recurrence was localized to the lymph nodes of the neck, and to determine the best strategy for further treatment. Between 1989 and 2001, 270 patients with mid- and lower-thoracic esophageal cancer underwent curative esophagectomy; 90 of those patients had a cancer recurrence. Our focus was on lymph node recurrence, especially when the recurrent cancers were localized to the lymph nodes in the neck. The outcomes of those patients and the efficacy of the strategies used to treat the recurrent cancers were determined. In 43 patients (48%), recurrent cancer initially appeared in the lymph nodes. Among the 43 patients, 15 (35%) had localized neck recurrence. The time between tumor recurrence and death among the 15 patients with localized neck recurrence was significantly longer than among the 28 patients with other recurrence patterns. In addition, 15 patients underwent lymph node resection, while 28 patients were treated non-surgically. The time between tumor recurrence and death was significantly longer in patients treated surgically. Of the 15 patients in whom recurrence affected the neck lymph nodes only, 10 (67%) were treated surgically; their 2-year survival rate after recurrence was 45%. The outcomes of recurrent esophageal cancers localized to the lymph nodes of the neck were better than those seen with other recurrence patterns, and salvage resection followed by chemoradiation therapy would seem to be indicated for those patients.

Survival Advantage of Using Autologous Blood Transfusion During Surgery for Esophageal Cancer

Abstract.Purpose: There is evidence that blood transfusion is associated with an increased rate of tumor recurrence. This study was conducted to assess the survival advantage of giving autologous blood instead of allogeneic blood during surgery for esophageal cancer. Methods: We retrospectively analyzed 62 patients who underwent esophagectomy for thoracic esophageal cancer between January 1991 and February 1995 and received allogeneic blood transfusion, and 61 patients operated on between March 1995 and February 1998, who received autologous blood transfusion. The clinicopathological factors and survival rates were compared between the two groups. Results: The clinicopathological factors that influenced prognosis were similar in the two groups; however, a definite survival advantage was evident in the autologous blood transfusion group. According to multivariate analyses, the transfusion of allogeneic blood was an independent prognostic factor (P = 0.0222), as was the presence of metastatic lymph nodes. Patients who received allogeneic blood transfusions perioperatively had more than a twofold greater risk (Hazard ration 2.406) of death over patients who received autologous blood transfusions. Conclusion: Autologous blood transfusion appears to be an independent prognostic factor for the survival of patients with esophageal cancer.

Histological confirmation of healing of gastrobronchial fistula using a muscle flap

We report a case of gastrobronchial fistula that developed after esophagectomy for esophageal cancer. The fistula was repaired successfully by transposing a pectoralis major muscle flap. Complete healing was confirmed histologically by epithelialization of the fistula site and at autopsy 12 months after surgery. Muscle flap transposition effectively repairs gastrobronchial fistula.

Hydrogen peroxide derived from intestine through the mesenteric lymph induces lung edema after surgical stress

Compelling evidence indicates that the small intestine is the primary source of factors inducing lung injury after major surgery and that the lymphatic system is the major route by which these gut-derived factors reach the pulmonary circulation. This study investigated the mechanism of lung edema induced by surgical stress. After subjecting male, fasted, pathogen-free Sprague-Dawley rats to surgical stress (laparotomy and intestinal handling for 5 min), followed by ventilation for 5 h, we measured H2O2 production in the mucosa of small intestine and in the lung using 2′,7′-dichlorofluorescein and intravital fluorescence microscopy. In addition, H2O2 in mesenteric lymph was measured using a quantitative assay; lung permeability was assessed as a function of extravasation of Evans blue dye; neutrophil accumulation was visualized by intravital fluorescence microscopy and assessed as a function of myeloperoxidase activity; and TNF-&agr; levels were measured using a specific ELISA. The intensity of 2′,7′-dichlorofluorescein fluorescence in the mucosa of small intestine, H2O2 levels of mesenteric lymph, and lung permeability were all significantly higher in rats subjected to surgical stress than in control animals. Moreover, all of these effects were blocked by pretreatment with a specific xanthine oxidase inhibitor. Surgical stress did not increase neutrophil accumulation or TNF-&agr; production in the lung. In conclusion, surgical stress induces xanthine oxidase–dependent H2O2 production in the small intestine. The H2O2 then enters the mesenteric lymph and travels to the lung, where it increases capillary permeability and thus induces edema.

Hydrogen peroxide induces midzonal heat shock protein 72 and apoptosis in sinusoidal endothelial cells of hypoxic rat liver.

Objective: To investigate the heat shock protein (HSP) 72 expression and apoptosis induced by hydrogen peroxide in hypoxic rat liver. Design: Prospective control study using the isolated rat liver. Setting: Animal research facility. Subjects: Fasted, pathogen‐free specific, male Sprague‐Dawley rats. Interventions: A low‐flow hypoxia model was made by reducing an afferent pressure from 10 to 2.5 cm H2O, and by perfusing the isolated rat liver for 2 hrs. Measurement and Main Results: We investigated the hydrogen peroxide production by using the 2′‐7′ dichlorofluorescein image, the induction of HSP 72 by using immunohistochemistry, and apoptosis by using terminal deoxynucleotidyl transferase‐mediated dUTP‐digoxigenin nick end‐labeling method in the low flow hypoxic rat liver. In low‐flow hypoxia, hydrogen peroxide production, HSP 72 expression, and apoptosis were induced in the midzone of rat liver. Prevalence of HSP 72 expression was higher in the sinusoidal endothelial cells (SEC) than in the hepatocytes. All apoptotic cells were SEC with expression of HSP 72. Hydrogen peroxide was derived from hepatocytes. Pretreatment with the specific xanthine oxidase inhibitor, sodium(‐)‐8‐(3‐methoxy‐4‐phenylsulfinylphenyl) pyrazolo [1,5‐a]‐1,3,5‐triazine‐4‐olate monohydrate significantly attenuated hydrogen peroxide production, HSP 72 expression, and apoptosis of SEC in the midzone. Conclusion: Xanthine oxidase‐dependent hydrogen peroxide induces midzonal and SEC‐dominant HSP 72 expression and apoptosis in hypoxic rat liver.

Esophageal cancer associated with right aortic arch: report of two cases.

We report herein two cases of thoracic esophageal cancer with a right aortic arch. Both cases were elderly males who complained of dysphagia. Computed tomography and aortography revealed a right aortic arch with a mirror-image branching and a diverticulum of the right descending aorta in both cases. They underwent an esophagectomy and a mediastinal lymph node dissection in a left thoractomy, and we also added a median sternotomy in the second case for a lymph node dissection in the right mediastinum. The ductus arteriosus was divided in the first case, but he died of a rupture of the aortic diverticulum 13 months later. In conclusion, for a successful esophagectomy and mediastinal lymph node dissection, a median sternotomy should be added to the left thoractomy, while careful attention should also be paid to the aortic diverticulum and the ductus arteriosus.

Hydrogen peroxide-dependent declines in Bcl-2 induces apoptosis in hypoxic liver.

BACKGROUND Low-flow hypoxia induces xanthine oxidase-dependent hydrogen peroxide production by hepatocytes in the midzone of blood-perfused rat livers and apoptosis in sinusoidal endothelial cells (SECs). As Bcl-2 is a potent inhibitor of apoptotic cell death and is localized mainly in the inner mitochondrial membrane and crista, the purpose of this study was to determine whether cell-specific changes in mitochondrial Bcl-2 levels could account for the hypoxia-induced apoptosis in SECs. MATERIALS AND METHODS A low-flow hypoxia model was generated in isolated rat livers by reducing perfusate inflow pressure from 10 to 2.5 cmH2O for 2 h. Apoptosis was then evaluated using the TdT-mediated dUTP-digoxigenin nick end-labeling (TUNEL) method. Mitochondrial Bcl-2 protein levels were determined in hepatocytes and SECs using cryosectioning immunogold labeling electron microscopy.Results. TUNEL-positive nonparenchymal cells, identified as SECs, were observed predominantly in the midzone of low-flow hypoxic rat livers, whereas few parenchymal cells were stained. Mitochondrial Bcl-2 levels were higher in SECs than in hepatocytes under control conditions, but they declined significantly during hypoxia, though no morphological signs of apoptosis were apparent. In hepatocytes, by contrast, Bcl-2 levels were unaffected by hypoxia. Pretreatment with a specific xanthine oxidase inhibitor, sodium (-)-8-(3-methoxy-4-phenylsulfinylphenyl) pyrazolo [1,5-a]-1,3,5-triazine-4-olate monohydrate, which blocks production of hydrogen peroxide, also blocked both the hypoxia-induced apoptosis and the decline in mitochondrial Bcl-2 in SECs. CONCLUSION Hydrogen peroxide-dependent declines in Bcl-2 induce apoptosis in SECs in the hypoxic rat liver.

Does Central Venous Pressure Reflect the Circulating Blood Volume for the Decrement of Compliance Just After Esophagectomy

Abstract: This study investigates whether the pressure parameters obtained from the Swan-Ganz catheter (SGC) accurately reflect the circulating blood volume just after en bloc resection of the thoracic esophagus with regional lymph node dissection. It is well known that this operation induces severe hemodynamic changes and although the pressure parameters obtained from the SGC are an accepted means of monitoring circulating blood volume, we have often experienced a discrepancy between the SGC data and the clinical state. We examined the pressure parameters and diameter of the inferior vena cava (IVC) and left ventricle (LV), and the central venous compliance using SGC and echocardiography in ten patients who underwent esophagectomy for esophageal cancer. The central venous pressure, pulmonary arterial mean pressure, and pulmonary artery wedged pressure were significantly increased just after the operation compared with the preoperative levels, while the diameters of the IVC and LV decreased just after the operation. The compliances of the IVC decreased significantly just after the operation. The hemodynamic shift to the third space after esophagectomy induces decrement of the compliances of IVC. As the CVP does not always reflect the circulating blood volume, measuring the diameter of the IVC using echocardiography is extremely useful for monitoring circulating blood volume just after esophagectomy.