5 research outputs found

    Predicting blood loss in burn excisional surgery

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    Background: Blood loss during burn excisional surgery remains an important factor as it is associated with significant comorbidity, mortality and longer length of stay. Blood loss is, among others, influenced by length of surgery, burn size, excision size and age. Most literature available is aimed at large burns and little research is available for small burns. Therefore, the goal of this study is to investigate blood loss and develop a prediction model to identify patient at risk for blood loss during burn excisional surgery ≤ 10% body surface area. Study design and methods: This retrospective study included adult patients who underwent burn excisional surgery of ≤ 10% body surface area in the period 2013–2018. Duplicates, patients with missing data and delayed surgeries were excluded. Primary outcome was blood loss. A prediction model for per-operative blood loss (>250 ml) was built using a multivariable logistic regression analysis with stepwise backward elimination. Discriminative ability was assessed by the area under the ROC-curve in conjunction with optimism and calibration. Results: In total 269 patients were included for analysis. Median blood loss was 50 ml (0−150) / % body surface area (BSA) excised and 0.28 (0–0.81) ml / cm2. Median burn size was 4% BSA and median excision size was 2% BSA. Blood loss of> 250 ml was present in 39% of patients. The model can predict blood loss> 250 ml based on %BSA excised, length of surgery and ASA-score with an AUC of 0.922 (95% CI 0.883 – 0.949) and an AUC after optimism correction of 0.915. The calibration curve showed an intercept of 0.0 (95% CI −0.36 to 0.36) with a slope of 1.0 (95% CI 0.78–1.22). Conclusion: Median blood loss during burn excisional surgery of ≤ 10% BSA is 50 ml / % BSA excised and 0.28 ml / cm2 excised. However, a substantial part of patients is at risk for higher blood loss. The prediction model can predict P(blood loss>250 ml) with an AUC of 0.922, based on expected length of surgery, ASA-score and size of excision. The model can be used to identify patients at risk for significant blood loss (>250 ml)

    Reducing Colorectal Anastomotic Leakage with Tissue Adhesive in Experimental Inflammatory Bowel Disease

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    Background:Anastomotic leakage after gastrointestinal surgery remains a challenging clinical problem. This study aimed to investigate the effectiveness of TissuCol (fibrin glue), Histoacryl Flex (n-butyl-2-cyanoacrylate), and Duraseal (polyethylene glycol) on colorectal anastomotic healing during experimental colitis.Methods:We first performed colectomy 7 days after 10 mg trinitrobenzene sulfonic acid (TNBS)-induced colitis to validate a rat TNBS-colitis-colectomy model. Subsequently, this TNBS-colitis-colectomy model was used in 73 Wistar rats that were stratified into a colitis group (CG, no adhesive), a TissuCol group (TG), a Histoacryl group (HG), and a Duraseal group (DG). Anastomotic sealant was applied with one adhesive after constructing an end-to-end hand-sewn anastomosis. Clinical manifestations, anastomotic bursting pressure, and immunohistochemistry of macrophage type-one (M1) and type-two (M2) was performed on postoperative day (POD)3 or POD7.Results:TNBS-caused mucosal and submucosal colon damage and compromised anastomotic healing (i.e., abscess formation and low anastomotic bursting pressure). On POD3, higher severity of abscesses was seen in CG. Average anastomotic bursting pressure was 53.2 35.5 mm Hg in CG, which was significantly lower than HG (134.4 +/- 27.5 mm Hg) and DG (95.1 +/- 54.3 mm Hg) but not TG (83.4 +/- 46.7 mm Hg). Furthermore, a significantly higher M2/M1 index was found in HG. On POD7, abscesses were only seen in CG (6/9) but not in other groups; HG had the lowest severity of adhesion.Conclusions:We describe the first surgical IBD model by performing colectomy in rats with TNBS-induced colitis, which causes intra-abdominal abscess formation and compromises anastomotic healing. Anastomotic sealing with Histoacryl Flex prevents these complications in this model. Alternative activation of macrophages seems to be involved in its influence on anastomotic healing
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