Outcomes following laparoscopic transhiatal esophagectomy for esophageal cancer.

BACKGROUND: Most published minimally invasive esophagectomy techniques involve a multiple field approach, including laparoscopic and thoracoscopic esophageal mobilization. Laparoscopic transhiatal esophagectomy (LTE) should potentially reduce the complications associated with thoracotomy. This study aims to compare outcomes of LTE with open transhiatal esophagectomy (OTE) and en-bloc esophagectomy (EBE). METHODS: Retrospective chart review was performed on all patients who had an LTE for cancer between July 2008 and July 2012 at our institution. Data was compared with an historic cohort of patients who underwent OTE and EBE at the same institution from July 2002 to July 2008. RESULTS: There were 33 patients with LTE, compared with 60 patients with OTE and 139 with EBE. The presence of minor operative complications was similar (p = 0.36), but major complications were significantly less common in the LTE group (12, 23 and 33 %, respectively; p = 0.04). The median number of blood transfusions during hospitalization was significantly lower in the LTE group (0, 2.5 and 3, respectively; p = 0.005). Median tumor size was significantly smaller (1.5, 2.2, and 3 cm, respectively; p = 0.03), but the LTE group had a significantly higher percentage of patients with neoadjuvant treatment (39, 14 and 29 %, respectively; p = 0.008). Median lymph node yield for LTE was lower (24, 36 and 48, respectively; p < 0.0001), but the percentage of patients with positive nodes was similar (33, 33 and 39 %, respectively; p = 0.69). Mortality was equivalent among the groups (0, 2 and 4 %, respectively; p = 0.38). The median LOS for the LTE group was significantly lower (10, 13 and 15 days, respectively; p < 0.0001). Overall survival was not different between the three groups (p = 0.65), with median survival at 24 months of 70, 65 and 65 %, respectively. CONCLUSION: LTE can be performed safely with less major complications and shorter hospital stay than open esophagectomy. The reduced lymph-node harvest did not impact overall survival.

Lung epithelial and endothelial damage, loss of tissue repair, inhibition of fibrinolysis, and cellular senescence in fatal COVID-19.

Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is characterized by respiratory distress, multiorgan dysfunction, and, in some cases, death. The pathological mechanisms underlying COVID-19 respiratory distress and the interplay with aggravating risk factors have not been fully defined. Lung autopsy samples from 18 patients with fatal COVID-19, with symptom onset-to-death times ranging from 3 to 47 days, and antemortem plasma samples from 6 of these cases were evaluated using deep sequencing of SARS-CoV-2 RNA, multiplex plasma protein measurements, and pulmonary gene expression and imaging analyses. Prominent histopathological features in this case series included progressive diffuse alveolar damage with excessive thrombosis and late-onset pulmonary tissue and vascular remodeling. Acute damage at the alveolar-capillary barrier was characterized by the loss of surfactant protein expression with injury to alveolar epithelial cells, endothelial cells, respiratory epithelial basal cells, and defective tissue repair processes. Other key findings included impaired clot fibrinolysis with increased concentrations of plasma and lung plasminogen activator inhibitor-1 and modulation of cellular senescence markers, including p21 and sirtuin-1, in both lung epithelial and endothelial cells. Together, these findings further define the molecular pathological features underlying the pulmonary response to SARS-CoV-2 infection and provide important insights into signaling pathways that may be amenable to therapeutic intervention.