Objective: "Rediscovered" in 1976, transhiatal esophagectomy (THE) has been applicable in most situations requiring esophageal resection and reconstruction. The objective of this study was to review the authors' 30-year experience with THE and changing trends in its use. Methods: Using the authors' prospective Esophagectomy Database, this single institution experience with THE was analyzed retrospectively. Results: Two thousand and seven THEs were performed-1063 (previously reported) between 1976 and 1998 (group I) and 944 from 1998 to 2006 (group II), 24% for benign disease, 76%, cancer. THE was possible in 98%. Stomach was the esophageal substitute in 97%. Comparing outcomes between group I and group II, statistically significant differences (P Ͻ 0.001) were observed in hospital mortality (4% vs. 1%); adenocarcinoma histology (69% vs. 86%); use of neoadjuvant chemoradiation (28% vs. 52%); mean blood loss (677 vs. 368 mL); anastomotic leak (14% vs. 9%); and discharge within 10 days (52% vs. 78%). Major complications remain infrequent: wound infection/dehiscence, 3%, atelectasis/pneumonia, 2%, intrathoracic hemorrhage, recurrent laryngeal nerve paralysis, chylothorax, and tracheal laceration, Ͻ1% each. Late functional results have been good or excellent in 73%. Aggressive preoperative conditioning, avoiding the ICU, improved pain management, and early ambulation reduce length of stay, with 50% in group II discharged within 1 week. Conclusion: THE refinements have reduced the historic morbidity and mortality of esophageal resection. This largest reported THE experience reinforces the value of consistent technique and a clinical pathway in managing these high acuity esophageal patients.

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Objectives Vascular smooth muscle cells can undergo profound changes in phenotype, defined by coordinated repression of smooth muscle cell marker genes and production of matrix metalloproteinases in response to injury. However, little is known of the role of smooth muscle cells in aortic aneurysms. We hypothesized that smooth muscle cells undergo phenotypic modulation early in the development of aortic aneurysms. Methods Abdominal aortas from C57B6 mice (n = 79) were perfused with elastase or saline (control) and harvested at 1, 3, 7, or 14 days. Aortas were analyzed by means of quantitative polymerase chain reaction and immunohistochemistry for smooth muscle cell marker genes, including SM22A, smooth muscle α-actin, and matrix metalloproteinases 2 and 9. In complimentary experiments human aneurysms (n = 10) and control aorta (n = 10) were harvested at the time of surgical intervention and analyzed. Results By 14 days, aortic diameter was larger after elastase perfusion compared with control diameter (100% ± 9.6% vs 59.5% ± 18.9%, P = .0002). At 7 days, elastase-perfused mice had a 78% and 85% reduction in SM22α and smooth muscle α-actin expression, respectively, compared with that seen in control animals well before aneurysms were present, and these values remained repressed at 14 days. Immunohistochemistry confirmed less SM22α and smooth muscle α-actin in experimental aneurysms at 14 days in concert with increased matrix metalloproteinase 2 and 9 expression at 7 and 14 days. Similarly, human aneurysms had less SM22α and smooth muscle α-actin and increased matrix metalloproteinase 2 and 9 staining, compared with control values, as determined by means of quantitative polymerase chain reaction. Conclusions Aneurysms demonstrate smooth muscle cell phenotypic modulation characterized by downregulation of smooth muscle cell marker genes and upregulation of matrix metalloproteinases. These events in experimental models occur before aneurysm formation. Targeting smooth muscle cells to a reparative phenotype might provide a novel therapy in the treatment of aortic aneurysms.

Gastroesophageal reflux disease is very common after lung transplantation and appears to contribute to mortality and development of bronchiolitis obliterans syndrome. Fundoplication in lung transplant recipients with gastroesophageal reflux disease is associated with significant improvements in lung function, particularly if performed before the late stages of bronchiolitis obliterans syndrome.

No abstract

There is a high prevalence of GERD among selected lung transplant recipients who had pH studies performed and its presence is associated with worse pulmonary function. Future studies are needed to assess whether GERD contributes to the pathogenesis of bronchiolitis obliterans syndrome (BOS).

Rationale: We recently implicated a role for CD4 1 T cells and demonstrated elevated IL-17A expression in lung ischemia-reperfusion (IR) injury. However, identification of the specific subset of CD4 1 T cells and their mechanistic role in IR injury remains unknown. Objectives: We tested the hypothesis that invariant natural killer T (iNKT) cells mediate lung IR injury via IL-17A signaling. Methods: Mice underwent lung IR via left hilar ligation. Pulmonary function was measured using an isolated lung system. Lung injury was assessed by measuring edema (wet/dry weight) and vascular permeability (Evans blue dye). Inflammation was assessed by measuring proinflammatory cytokines in lungs, and neutrophil infiltration was measured by immunohistochemistry and myeloperoxidase levels. Measurements and Main Results: Pulmonary dysfunction (increased airway resistance and pulmonary artery pressure and decreased pulmonary compliance), injury (edema, vascular permeability), and inflammation (elevated IL-17A; IL-6; tumor necrosis factor-a; monocyte chemotactic protein-1; keratinocyte-derived chemokine; regulated upon activation, normal T-cell expressed and secreted; and neutrophil infiltration) after IR were attenuated in IL-17A 2/2 and Rag-1 2/2 mice. Anti-IL-17A antibody attenuated lung dysfunction in wildtype mice after IR. Reconstitution of Rag-1 2/2 mice with wild-type, but not IL-17A 2/2 , CD4 1 T cells restored lung dysfunction, injury, and inflammation after IR. Lung dysfunction, injury, IL-17A expression, and neutrophil infiltration were attenuated in Ja18 2/2 mice after IR, all of which were restored by reconstitution with wild-type, but not IL-17A 2/2 , iNKT cells. Flow cytometry and enzyme-linked immunosorbent spot assay confirmed IL-17A production by iNKT cells after IR.Conclusions: These results demonstrate that CD4 1 iNKT cells play a pivotal role in initiating lung injury, inflammation, and neutrophil recruitment after IR via an IL-17A-dependent mechanism.

Implementation of thoracic ERAS is a dynamic process with potential to improve outcomes in thoracic surgical procedures. In the first year we shortened length of stay, decreased opioid usage, minimized fluid overload, and decreased hospital costs.