First experiences with the Radial Reload with Tri-staple (TM) technology in low rectal surgery

INTRODUCTION: Low rectal surgery remains challenging. New surgical stapler devices have been developed to counteract problems of impaired visibility and inability to get low into the pelvis. One of them is the Radial Reload (RR) with Tri-staple() Technology (Covidien, New Haven, CT, USA). The aim of this study was to assess the first impressions and experiences regarding handling of this new stapler device in low anterior resection procedures in living humans. METHODS: A questionnaire, consisting of 27 statements concerning accessibility, maneuverability and visibility, was sent to 35 surgeons worldwide. RESULTS: A total of 85 rectal surgical procedures, both open and laparoscopic, were assessed by 31 surgeons. In 97% of the procedures the surgeons agreed that the RR stapler device facilitated access in the low pelvis. The first stapler device firing achieved complete transection in 54% of the procedures. According to the surgeons' assessments, in 91% percent of the procedures the RR stapler device enabled creation of adequate margins. Visualization of the pelvic floor was reported in 93% of the procedures. In the surgeons' opinion, the RR stapler device was considered clinically acceptable in 93% of the procedures. In 79% of the procedures the surgeon preferred the RR stapler device over the stapler device they normally used. CONCLUSION: This study showed that the first experiences with the RR stapler device of 33 surgeons in 85 low rectal procedures are positive. It facilitates low stapling in both open and laparoscopic procedures. Good visibility, maneuverability and the possibility to create adequate distal margins were reported

Enterocyte shedding and epithelial lining repair following ischemia of the human small intestine attenuate inflammation

BACKGROUND: Recently, we observed that small-intestinal ischemia and reperfusion was found to entail a rapid loss of apoptotic and necrotic cells. This study was conducted to investigate whether the observed shedding of ischemically damaged epithelial cells affects IR induced inflammation in the human small gut. METHODS AND FINDINGS: Using a newly developed IR model of the human small intestine, the inflammatory response was studied on cellular, protein and mRNA level. Thirty patients were consecutively included. Part of the jejunum was subjected to 30 minutes of ischemia and variable reperfusion periods (mean reperfusion time 120 (+/-11) minutes). Ethical approval and informed consent were obtained. Increased plasma intestinal fatty acid binding protein (I-FABP) levels indicated loss in epithelial cell integrity in response to ischemia and reperfusion (p<0.001 vs healthy). HIF-1alpha gene expression doubled (p = 0.02) and C3 gene expression increased 4-fold (p = 0.01) over the course of IR. Gut barrier failure, assessed as LPS concentration in small bowel venous effluent blood, was not observed (p = 0.18). Additionally, mRNA expression of HO-1, IL-6, IL-8 did not alter. No increased expression of endothelial adhesion molecules, TNFalpha release, increased numbers of inflammatory cells (p = 0.71) or complement activation, assessed as activated C3 (p = 0.14), were detected in the reperfused tissue. CONCLUSIONS: In the human small intestine, thirty minutes of ischemia followed by up to 4 hours of reperfusion, does not seem to lead to an explicit inflammatory response. This may be explained by a unique mechanism of shedding of damaged enterocytes, reported for the first time by our group

Enhancing intestinal anastomotic healing using butyrate: Systematic review and meta-analysis of experimental animal studies.

BACKGROUND: Despite advancements in surgical technique and perioperative care, intestinal anastomoses still have a 10-15 per cent risk of leakage, which results in considerable morbidity and/or mortality. Recent animal studies have suggested that administration of butyrate to the anastomotic site results in enhanced anastomotic strength, which may prevent leakage. This systematic review and meta-analysis summarises current evidence concerning the effect of butyrate administration on anastomotic healing and will form a scientific basis for the development of new research into this subject. METHODS: Animal studies on the effect of butyrate-based interventions in models of intestinal anastomotic healing were systematically retrieved from online databases. Bibliographical data, study characteristics and outcome data were extracted, and internal validity of the studies was assessed. Outcomes studied through meta-analysis concerned: anastomotic strength, anastomotic leakage, collagen metabolism and general histologic parameters of wound healing. RESULTS: A comprehensive search and selection identified 19 relevant studies containing 41 individual comparisons. Design and conduct of most experiments were poorly reported resulting in an unclear risk of bias. Meta-analyses showed that butyrate administration significantly increases anastomotic strength (SMD 1.24, 0.88 to 1.61), collagen synthesis (SMD 1.44, 0.72 to 2.15) and collagen maturation, making anastomoses less prone to leakage in the early postoperative period (OR 0.37, 0.15 to 0.93). CONCLUSION: This systematic review and meta-analysis shows that there is potential ground to investigate the use of butyrate in clinical trials to prevent anastomotic leakage in intestinal surgery. However, more research is necessary to define the best application form, dosage and administration route

A new model to study intestinal ischemia-reperfusion damage in man.

BACKGROUND: This report describes a human in vivo ischemia reperfusion (IR) model of the small intestine. Animal models of intestinal IR are indispensable for our understanding of sequelae of IR induced organ damage. However, a functional experimental IR model of the human small intestine, allowing for translational research, can be considered critical for our pathophysiologic understanding of intestinal IR in man. MATERIALS AND METHODS: Patients with a healthy gut undergoing abdominal surgery with a Roux-Y or similar reconstruction were included, creating the opportunity to study IR of an isolated jejunal segment in a harmless model. RESULTS: Ischemia was induced by nontraumatic vascular clamping followed by reperfusion. This model can be adapted using variable ischemia and reperfusion times. Similarly, tissue and plasma can be collected at any given time point during ischemia until end of reperfusion, only determined by progress of the original, intended surgical procedure. CONCLUSION: A unique and harmless human IR model of the jejunum was created, which enables the study of acute damage to the epithelial lining and its subsequent repair mechanisms

Intestinal cytoskeleton degradation precedes tight junction loss following hemorrhagic shock.

Hemorrhagic shock (HS) leads to intestinal barrier loss, causing systemic inflammation, which in turn can ultimately lead to multiorgan dysfunction syndrome. Barrier function is based on tight junctions (TJs) between intact epithelial cells. These TJs are anchored in the cell via the filamentous actin (F-actin) cytoskeleton. We hypothesize that HS causes hypoperfusion, leading to loss of F-actin, via activation of actin-depolymerizing factor/cofilin (AC), and consequently TJ loss. This study is aimed at unraveling the changes in cytoskeleton and TJ integrity after HS in organs commonly affected in multiorgan dysfunction syndrome (liver, kidney, and intestine) and to elucidate the events preceding cytoskeleton loss. Adult rats were subjected to a nonlethal HS and killed, along with unshocked controls, at 15, 30, 60, and 90 min after induction of shock. Cytoskeleton, TJ integrity loss, and its consequences were studied by assessment of globular actin, F-actin, AC, zonula occludens protein 1, claudin 3, and bacterial translocation. In the liver and kidney, TJ and the F-actin cytoskeleton remained intact at all time points studied. However, in the intestine, significant loss of F-actin and increase of globular actin was seen from 15 min after shock. This change preceded statistically significant loss of the TJ proteins claudin 3 and zonula occludens protein 1, which were observed starting at 60 min after induction of shock (P &lt; 0.05 vs. controls). Early after induction of shock (15 and 30 min) the nonactive AC (phosphorylated AC) in the intestine was significantly decreased (by 21% and 27%, P &lt; 0.05 vs. control), whereas total AC remained constant, reflecting an increase in activated AC in the intestine from 15 min after shock. Bacterial translocation to mesenteric lymph nodes, liver, and spleen was present from 30 min after shock. This study shows for the first time that HS results in AC activation, selective intestinal actin cytoskeleton disruption, and TJ loss very early after the onset of shock. Loss of this intestinal barrier results in translocation of toxins and bacteria, which enhances inflammation and leads to infections

Sarcopenia is highly prevalent in patients undergoing surgery for gastric cancer but not associated with worse outcomes

OBJECTIVES: Aim of this study was to assess the prevalence of sarcopenia and body composition (i.e., subcutaneous and visceral fat) in gastric cancer surgical patients and its association with adverse postoperative outcome. METHODS: Preoperative CT scans were obtained from all patients who underwent surgery for gastric adenocarcinoma between January 2005 and September 2012. Total muscle and adipose tissue cross-sectional area were measured at the level of the third lumbar vertebra (L3) transverse processes. Sarcopenia was defined according to gender- and body mass index (BMI)-specific cutoff points. Primary outcome was in-hospital mortality. Secondary outcomes were severe postoperative complications (i.e., Clavien-Dindo classification >/=3a complications) and 6-month mortality. RESULTS: In 152 out of a total of 180 (84.4%) patients, a CT-scan was available for analysis. In total, 86 (57.7%) of the patients were classified as sarcopenic. Sarcopenia was no predictor for in-hospital mortality (P = 0.52), severe complications (P = 1.00) or 6-month mortality (P = 0.69). Intraabdominal and subcutaneous adipose tissue measurements were not associated with in-hospital mortality, severe complications or 6-month mortality. CONCLUSIONS: In this population of gastric cancer surgical patients, the prevalence of sarcopenia was 57.7%, which is high compared to other abdominal surgical oncology populations. However, sarcopenia was not associated with postoperative morbidity or mortality

Gut mucosal cell damage in meningococcal sepsis in children: relation with clinical outcome.

OBJECTIVE:: The pathophysiological sequelae of meningococcal sepsis are mainly caused by deregulated microvasculature function, leading to impaired tissue blood flow. Because mature enterocytes are known to be susceptible to altered perfusion, we aimed to investigate: (1) the development of enterocyte damage; and (2) the relation between enterocyte damage and severity of disease and outcome in children with meningococcal sepsis. DESIGN:: Retrospective human study. SETTING:: Pediatric intensive care unit at a university hospital. PATIENTS:: Nineteen consecutive children with meningococcal sepsis were studied during their pediatric intensive care unit stay. INTERVENTIONS:: None. MEASUREMENT AND MAIN RESULTS:: Circulating levels of intestinal fatty acid binding protein, a small cytosolic protein constitutively present in mature enterocytes and released on cell injury, were assessed. Severity of disease was represented by meningococcal-specific Rotterdam Score, generic Pediatric Risk of Mortality II score, and circulating interleukin-6. Clinical outcome was measured by length of pediatric intensive care unit stay and number of ventilator days. Highest plasma intestinal fatty acid binding protein values were measured on pediatric intensive care unit stay admission. At the time of admission, eight of 19 patients had higher intestinal fatty acid binding protein plasma levels than the upper reference limit of 30 healthy volunteers. In all survivors, intestinal fatty acid binding protein levels declined to normal values within 12 hrs after starting intensive treatment, whereas the three nonsurvivors maintained elevated intestinal fatty acid binding protein plasma levels. A significant correlation was found among intestinal fatty acid binding protein and Rotterdam Score, Pediatric Risk of Mortality II, interleukin-6 at admission (Spearman's r = 0.402, p = 0.006; r = 0.243, p = 0.045; r = 0.687, p < 0.001, respectively). Next, a significant correlation was found between intestinal fatty acid binding protein and clinical outcome. CONCLUSIONS:: Elevated plasma intestinal fatty acid binding protein is found in eight of 19 children with severe pediatric intensive care unit stay at the time of clinical presentation, suggesting the presence of enterocyte damage. Furthermore, prolonged enterocyte damage is found in nonsurvivors. Further studies are needed to clarify the potential role for assessment of plasma intestinal fatty acid binding protein in monitoring treatment of pediatric intensive care unit stay