OBJECTIVE:Colorectal cancer (CRC) is the third most diagnosed cancer, and requires surgical resection and reconnection, or anastomosis, of the remaining bowel to re-establish intestinal continuity. Anastomotic leak (AL) is a major complication that increases mortality and cancer recurrence. Our objective is to assess the causal role of gut microbiota in anastomotic healing. DESIGN:The causal role of gut microbiota was assessed in a murine AL model receiving faecal microbiota transplantation (FMT) from patients with CRC collected before surgery and who later developed or not, AL. Anastomotic healing and gut barrier integrity were assessed after surgery. Bacterial candidates implicated in anastomotic healing were identified using 16S rRNA gene sequencing and were isolated from faecal samples to be tested both in vitro and in vivo. RESULTS:Mice receiving FMT from patients that developed AL displayed poor anastomotic healing. Profiling of gut microbiota of patients and mice after FMT revealed correlations between healing parameters and the relative abundance of Alistipes onderdonkii and Parabacteroides goldsteinii. Oral supplementation with A. onderdonkii resulted in a higher rate of leaks in mice, while gavage with P. goldsteinii improved healing by exerting an anti-inflammatory effect. Patients with AL and mice receiving FMT from AL patients presented upregulation of mucosal MIP-1α, MIP-2, MCP-1 and IL-17A/F before surgery. Retrospective analysis revealed that patients with AL present higher circulating neutrophil and monocyte counts before surgery. CONCLUSION:Gut microbiota plays an important role in surgical colonic healing in patients with CRC. The impact of these findings may extend to a vast array of invasive gastrointestinal procedures.

In our recent publication in Gut, we showed that preoperative gut microbiota was causally linked to the development of anastomotic leak (AL) after colorectal cancer (CRC) surgery. AL results from impaired healing of the colonic wound and leads to the leakage of intestinal content into the abdomen. Using faecal microbiota transplantation (FMT) in mice with faecal samples from 18 patients with CRC, we established that preanastomosis expression of mucosal proinflammatory cytokines, namely macrophage inflammatory protein1 alpha (MIP1α), monocyte chemoattractant protein1 (MCP1), macrophage inflammatory protein 2 (MIP2) and interleukin17A/F (IL17A/F), was increased in patients who later developed AL. Most importantly, these higher basal cytokine levels were driven by gut microbiota, as FMT from these patients led to higher cytokine levels in mice. To corroborate these findings, we now expanded the analysis to our cohort of 77 patients with CRC who underwent a bowel resection with anastomosis (table 1): 13 were diagnosed with poor anastomotic healing and AL after surgery or at followup, while 64 did not. Colonic mucosal biopsies were collected during surgery from all patients and the levels of nine cytokines were measured (online supplemental material), confirming higher levels of MIP1α, MIP2, MCP1 and IL17A/F in patients who later developed AL (figure 1A). This larger cohort also revealed that the basal levels of IL1β and tumour necrosis factor alpha, which we have previously shown to be increased after surgery in patients with AL, were already high before completion of the anastomosis. Proinflammatory IL5 and interferongamma were also increased at baseline. Antiinflammatory IL10 was also high in AL patients, probably as a feedback mechanism due to higher inflammation. As mucosal cytokines cannot be easily assessed in clinical practice, we quantified proinflammatory markers in preoperative faecal samples. Calprotectin is a faecal marker routinely used in patients with inflammatory bowel disease, and we have shown that lipocalin2 (LCN2) correlates with circulating white blood cells. Both markers were increased before surgery in patients with poor healing and leakage after surgery (figure 1B), and significantly correlated with postoperative levels of serum Creactive protein, a marker routinely measured after surgery for early detection of AL (figure 1C,D). Thus, calprotectin and LCN2 may be used as predictive markers of AL before surgery. Using receiver operating characteristic curves to assess the predictive capacity of these markers, we found that LCN2 performed better with a greater area under the curve (figure 1E). Moreover, LCN2 is a highly sensitive marker for very low levels of lowgrade inflammation. These findings reinforce the hypothesis that preoperative, lowgrade colonic inflammation may drive AL after colorectal surgery. Subclinical inflammation is increasingly recognised as a potential driver of poor anastomotic healing in bowel surgery. In keeping with our findings, a recent report showed that preoperative levels of circulating white cells were higher in patients that developed AL after colorectal surgery. Another study suggested that serum chemokine levels were higher before surgery in patients experiencing AL, and more evidence has emerged on the impact of preoperative lowgrade inflammation on AL in gastric and oesophageal surgery. 9 Our analysis is the first to demonstrate the role of preoperative mucosal proinflammatory signals in the pathogenesis of AL, and highlights the importance of gut bacteria in modulating these signals. As a proof of concept, we investigated whether preoperative calprotectin and LCN2 levels could predict patients at risk of complications. Both markers were high in AL patients at baseline, but LCN2 displayed a greater difference before surgery with a better predictive performance. These findings stress the urgency of implementing preoperative noninvasive tools to quantify lowgrade inflammation to identify in advance patients who are at risk of poor outcomes. This paves the way towards preventive microbiotamodifying interventions to promote gut repair and anastomotic healing.

Background The standard of care of colorectal cancer (CRC) management consists of surgical resection of the colon or rectum, followed by a reconnection, or ‘anastomosis’, of the remaining bowel ends to re-establish gastrointestinal continuity. Up to 30% of patients may present poor healing of the anastomosis, and anastomotic leak (AL), a major complication that increases mortality and morbidity after surgery. Our objective is to investigate the possible role of the gut microbiome in anastomotic healing in patients with CRC. Methods Preoperative fecal samples were collected from CRC patients undergoing surgery. The gut microbiota of patients with AL and of others that presented optimal healing were analyzed and compared using the Anchor pipeline. Fecal microbiota transplantation (FMT) was performed in mice using preoperative fecal samples from CRC patients with and without AL. Mice were then subjected to colonic surgery using a colonic anastomosis model. After 6 days, anastomotic healing and the gut barrier were assessed. The gut microbiota composition was compared as well to detect potential differences between the groups of mice transplanted from donors with and without AL. Results Mice colonized by FMT with the microbiota of donors with AL displayed macroscopically poorer healing of the colonic anastomosis and a higher bacterial translocation to the spleen, suggestive of a weaker gut barrier after surgery. The anastomotic wounds of mice receiving the microbiota of AL donors displayed lower concentrations of collagen and fibronectin and higher inflammatory cytokines, indicating poor extracellular matrix formation after surgery. This was accompanied by a higher expression of collagenolytic enzymes, indicative of collagen degradation at the wound site. The beta diversity of the gut microbiota was significantly different between mice receiving the microbiota of donors with and without AL. Several bacterial species were differentially abundant between the two groups and were associated with the healing process. Conclusions The preoperative gut microbiota in CRC patients with poor postoperative healing induces poor healing in mice and a weaker gut barrier after surgery. These results suggest a causal role for the gut microbiota in colonic healing after surgery in patients with CRC.

# 01. Operative classification of ventral abdominal hernias: new and practical classification {#article-title-2} Ventral hernias of the abdomen are defined as a noninguinal, nonhiatal defect in the fascia of the abdominal wall. Unfortunately, there is not currently a universal classification system

Introduction In addition to attacking the respiratory system, the coronavirus disease may attack the gastrointestinal tract in various ways, one of which is by creating a coagulopathy that may lead to acute ischemia of the bowel, increasing morbidity and mortality rates in these patients. Presentation of case We present a case of a white 72-year-old European male, who was admitted to the intensive care unit after developing COVID-19-induced acute respiratory distress syndrome. On the third week, despite a favorable evolution of his respiratory symptoms, the patient became clinically septic; laboratory findings showed an augmentation of his d -dimer, fibrinogen, C-reactive protein, and procalcitonin levels. Imaging showed signs of ischemia of the right colon. The patient was taken to the operating room; only the right side of his colon was ischemic, with a well demarcated cut-off. A laparoscopic right hemicolectomy with a terminal ileostomy was performed. The patient was able to go home 2 weeks after surgery. Discussion and conclusion Ischemic colitis is an uncommon pathology in the general population, and is rare in COVID-19 patients. Most cases of ischemic colitis in COVID-19 patients in the literature were limited to the left colon, with < 10 cases involving the right colon. Accurate and quick diagnosis with appropriate management is the key to avoid any mortality in those patients who are already weakened by the coronavirus.

Sclerosing encapsulating peritonitis (SEP) is a whitish fibrous envelope that encapsulates intra-abdominal peritonealized organs. Although it pathophysiology is not well understood, several possible causes have been reported in the literature, including peritoneal dialysis, past abdominal surgeries, peritonitis, beta-blockers and peritoneal carcinomatosis (PC). Some idiopathic cases, with no apparent causes, were described. We present a SEP case in a 43-year-old woman with a surgical history of pancreatic and liver resection for metastatic pseudopapillary pancreatic tumor, followed by several peritonectomies for PC. She was admitted for acute-on-chronic small-bowel obstruction that did not resolve with conservative management. Surgical exploration revealed a fibrous sheath covering the small-bowel. Extensive dissection, along with small-bowel segmental resection and anastomosis, was performed. The specimen was cancer-free. The mechanism through which SEP develops in certain surgical patients is still unknown. This report presents a case of successful surgical management and a review of the literature.

e15692 Background: Watch and wait protocol in patients with complete clinical response after neo-adjuvant therapy for rectal cancer has shown encouraging results with adequate follow up, allowing patients to avoid morbidities related to surgery. Methods: Retrospective study Between April 2008 and May 2017 was conducted in our center. 36 patients with rectal cancer of stage I to III according to UICC, treated with neo-adjuvant radiochemotherapy RCT, radio brachytherapy R-BT, brachytherapy BT, and brachy-chemotherapy BCT that had CCR were included. CCR was identified through digital rectal examination, endoscopy and MRI. Follow up was set according to guidelines reported in literature. Each patient had digital rectal examination, flexible recto-sigmoidoscopy with/without biopsy, and MRI every 3 months for the first 2 years. Results: 36 patients were included. Initial stage was assessed with MRI in 32 patients and ERUS in 23 patients. 8.3% were stage I, 63.9% stage II, 27.8% stage III. The mean distance from anal margin was 5cm. The neo-adjuvant protocol was RCT in 77.8%, R-BT in 5.6%, BT in 13.9%, and BCT in 2.7%. Patients were assessed for tumor response at an average of 8.2 weeks from the end of the treatment. 6 patients were operated for local recurrences 16.6%. All local recurrences were diagnosed within the first year. The overall morbidity in the operated patients was acceptable. The complications were class I Clavien-Dindo 57% in 4 patients, 1 patient had class II complication 14%, 1 patient had class III complication 14%, and 1 patient had class IV complication 14%. 50% of the patients had positive surgical resection margin. 1 patient had complete pathological response on the histopathology. Conclusions: Concomitant RCT offers better outcome in terms of CCR than RT alone. Watch and wait management of rectal cancer with CCR was feasible with a well-designed follow up protocol. ?In our study we were limited by the short period of follow up and the small effective. Our results are comparable to results reported in literature.