Textbook outcome after esophagectomy: A retrospective study from a high-volume center.

BACKGROUND: Textbook outcome is a composite quality measurement in esophageal cancer surgery. This study aimed to estimate the rate of textbook outcome esophagectomies at a high-volume center and investigate associations between textbook outcome and overall and recurrence-free survival. METHODS: A retrospective single-center study was conducted at Copenhagen University Hospital, Rigshospitalet, Denmark, analyzing esophagectomies performed from November 1, 2016, to December 31, 2021. Patients with primary carcinoma of the gastroesophageal junction who underwent elective and curative esophagectomy were included. The rate of textbook outcome esophagectomies was calculated, and the impact of textbook outcome on overall and recurrence-free survival was analyzed using Kaplan-Meier and Cox regression. RESULTS: A total of 433 patients were included in the study. Textbook outcome was achieved in 195 patients (45%). Achieving textbook outcome was independently associated with improved overall survival (HR 0.67; P = .011) and with a median overall survival of 57 months and 32 months for patients with or without textbook outcome, respectively. A trend for improved recurrence-free survival was observed for patients with textbook outcome (HR 0.74; P = .064). CONCLUSION: The present study found a consensus-based textbook outcome rate of 45%. Textbook outcome was found to be directly associated with improved overall survival. These results emphasize the association between improved short-term outcomes and long-term survival.

Major open abdominal surgery is associated with increased levels of endothelial damage and interleukin-6.

OBJECTIVE: To examine changes in biomarkers of endothelial glycocalyx shedding, endothelial damage, and surgical stress following major open abdominal surgery and the correlation to postoperative morbidity. INTRODUCTION: Major abdominal surgery is associated with high levels of postoperative morbidity. Two possible reasons are the surgical stress response and the impairment of the glycocalyx and endothelial cells. Further, the degree of these responses may correlate with postoperative morbidity and complications. METHODS: A secondary data analysis of prospectively collected data from two cohorts of patients undergoing open liver surgery, gastrectomy, esophagectomy, or Whipple procedure (n = 112). Hemodynamics and blood samples were collected at predefined timestamps and analyzed for biomarkers of glycocalyx shedding (Syndecan-1), endothelial activation (sVEGFR1), endothelial damage (sThrombomodulin (sTM)), and surgical stress (IL6). RESULTS: Major abdominal surgery led to increased levels of IL6 (0 to 85 pg/mL), Syndecan-1 (17.2 to 46.4 ng/mL), and sVEGFR1 (382.8 to 526.5 pg/mL), peaking at the end of the surgery. In contrast, sTM, did not increase during surgery, but increased significantly following surgery (5.9 to 6.9 ng/mL), peaking at 18 h following the end of surgery. Patients characterized with high postoperative morbidity had higher levels of IL6 (132 vs. 78 pg/mL, p = 0.007) and sVEGFR1 (563.1 vs. 509.4 pg/mL, p = 0.045) at the end of the surgery, and of sTM (8.2 vs. 6.4 ng/mL, p = 0.038) 18 h following surgery. CONCLUSION: Major abdominal surgery leads to significantly increased levels of biomarkers of endothelial glycocalyx shedding, endothelial damage, and surgical stress, with the highest levels seen in patients developing high postoperative morbidity.

Laser Speckle Contrast Imaging-based diagnosis of severe mesenteric traction syndrome: Hemodynamics and prostacyclin - A prospective cohort study.

BRIEF ABSTRACT: Today, the diagnosis and grading of mesenteric traction syndrome relies on a subjective assessment of facial flushing. However, this method has several limitations. In this study, Laser Speckle Contrast Imaging and a predefined cut-off value are assessed and validated for the objective identification of severe mesenteric traction syndrome. BACKGROUND: Severe mesenteric traction syndrome (MTS) is associated with increased postoperative morbidity. The diagnosis is based on an assessment of the developed facial flushing. Today this is performed subjectively, as no objective method exists. One possible objective method is Laser Speckle Contrast Imaging (LSCI), which has been used to show significantly higher facial skin blood flow in patients developing severe MTS. Using these data, a cut-off value has been identified. This study aimed to validate our predefined LSCI cut-off value for identifying severe MTS. METHODS: A prospective cohort study was performed on patients planned for open esophagectomy or pancreatic surgery from March 2021 to April 2022. All patients underwent continuous measurement of forehead skin blood flow using LSCI during the first hour of surgery. Using the predefined cut-off value, the severity of MTS was graded. In addition, blood samples for prostacyclin (PGI2) analysis and hemodynamics were collected at predefined time points to validate the cut-off value. MAIN RESULTS: Sixty patients were included in the study. Using our predefined LSCI cut-off value, 21 (35 %) patients were identified as developing severe MTS. These patients were found to have higher concentrations of 6-Keto-PGFaα (p = 0.002), lower SVR (p < 0.001), lower MAP (p = 0.004), and higher CO (p < 0.001) 15 min into surgery, as compared with patients not developing severe MTS. CONCLUSION: This study validated our LSCI cut-off value for the objective identification of severe MTS patients as this group developed increased concentrations of PGI2 and more pronounced hemodynamic alterations compared with patients not developing severe MTS.

Evaluation of the systemic inflammatory response, endothelial cell dysfunction, and postoperative morbidity in patients, receiving perioperative corticosteroid, developing severe mesenteric traction syndrome - an exploratory study.

OBJECTIVE: To determine whether a severe mesenteric traction syndrome (MTS) leads to increased surgical stress, endothelial dysfunction, and postoperative morbidity in a cohort in which all patients received a single dose of methylprednisolone. INTRODUCTION: Preoperatively administered corticosteroids lower the incidence of severe MTS and may also attenuate surgical stress and endothelial damage associated with the development of severe MTS, ultimately lowering the postoperative morbidity. METHODS: This exploratory study analyzed prospectively collected data from 45 patients all receiving 125 mg methylprednisolone. No control group was included. The severity of MTS was graded intraoperatively, and postoperative morbidity was assessed blinded. Blood samples for plasma prostacyclin (PGI2), IL6 and endothelial damage (Syndecan-1, sVEGRF1 and sThrombomodulin) biomarkers were obtained at predefined time points. RESULTS: Patients undergoing either open liver surgery (n = 23) or Whipple's procedure (n = 22) were included. No differences were found in postoperative morbidity between patients developing and not developing severe MTS. Surgery led to significantly increased plasma levels of biomarkers indicative of surgical stress and endothelial damage. Further, patients developing severe MTS had increased levels of PGI2 (p = 0.05) and lower systemic vascular resistance (p < 0.05) 15 min into surgery. However, when comparing the biomarkers of surgical stress, endothelial damage no differences between patients with and without severe MTS were identified. CONCLUSION: This exploratory study found that surgery was associated with a pro-inflammatory response and damage to the endothelium. However, no differences were found between patients developing severe MTS and patients developing moderate/no MTS in biomarkers of surgical stress, endothelial damage, or postoperative morbidity. Corticosteroids may therefore attenuate the endothelial damage in patients developing severe MTS. However, as this was an exploratory study, these findings must be confirmed in future randomized controlled studies.

Severe mesenteric traction syndrome is associated with increased systemic inflammatory response, endothelial dysfunction, and major postoperative morbidity.

This study aimed to determine if mesenteric traction syndrome (MTS) triggers increased systemic inflammation and endothelial cell dysfunction. Patients developing severe MTS had pronounced early IL6 elevations followed by endothelial cell damage. Furthermore, these processes were associated with increased postoperative morbidity. OBJECTIVE: To determine whether mesenteric traction syndrome (MTS) leads to increased systemic inflammation and dysfunction of the glycocalyx and endothelial cell and whether this correlates with the degree of postoperative morbidity. INTRODUCTION: Severe MTS is associated with increased postoperative morbidity following major gastrointestinal surgery, but the pathophysiological mechanism has not been previously explored. Systemic inflammatory response and impaired glycocalyx and endothelial cells may be responsible for the development of symptoms. METHODS: The study analyzed prospectively collected data from two cohorts (n = 67). The severity of the MTS response was graded intraoperatively and blood samples for PGI2, catecholamines, IL6, and endothelial biomarkers obtained at predefined time points. RESULTS: Patients undergoing either esophagectomy (n = 45) or gastrectomy (n = 22) were included. Surgery led to significantly increased plasma concentrations of all biomarkers. Yet, patients who developed severe MTS had higher baseline epinephrine levels (p < 0.05) and higher levels of PGI2 (p < 0.05), Syndecan-1 (p < 0.001), and sVEGFR1 (p < 0.001). Peak values of IL6, Syndecan-1, sVEGFR1, and sTM all correlated to peak PGI2. Lastly, patients with high postoperative morbidity had higher baseline epinephrine (p = 0.009) and developed higher plasma IL6 (p = 0.007) and sTM (p = 0.022). CONCLUSION: The development of severe MTS during upper gastrointestinal surgery is associated with preoperative elevated plasma epinephrine and further a more pronounced proinflammatory response and damage to the vascular endothelium. The increased postoperative morbidity seen in patients with severe MTS may thus, in part, be explained by an inherent susceptibility towards an inappropriate secretion of PGI2, which leads to an increased surgical stress response and endothelial damage. These findings must be confirmed in a new prospective cohort.