Septic shock reduces intestinal microcirculation and anastomotic perfusion: A porcine laser speckle contrast imaging study
Year: 2026
Type: article
Abstract: BACKGROUND Septic shock disrupts systemic and organ-specific microcirculation, leading to poor tissue perfusion and impaired healing. While mesenteric hemodynamics have been studied, the impact of sepsis on intestinal microcirculation and anastomotic healing remains unclear. AIM To assess the short-term effects of septic shock on microcirculation in the small intestine and colon, with a focus on hand-sewn and stapled anastomoses, using laser speckle contrast imaging (LSCI). METHODS Ten pigs underwent midline laparotomy with the creation of four anastomoses: One hand-sewn and one stapled anastomosis in both the small intestine and colon. LSCI measurements were taken before anastomosis formation (TB), immediately after (TA), and after one hour of rest (T0). Septic shock was induced via intravenous Escherichia coli infusion, with subsequent LSCI measurements at 30-minute intervals (T30-T150). Results were expressed as relative changes compared to TB. RESULTS Septic shock significantly reduced microcirculation in both untouched intestine and anastomoses. Hand-sewn anastomoses consistently exhibited higher perfusion than stapled anastomoses. At T150, perfusion in hand-sewn anastomoses remained significantly higher than in stapled anastomoses (51% vs 34% of TB, P = 0.002). CONCLUSION This study shows that septic shock significantly impairs intestinal microcirculation indicating a risk of intestinal ischemia if bacteriaemia and subsequent septic shock is untreated. Due to diminish blood flow following septic shock, the anastomotic healing may be compromised leading to increased risk of anastomotic leakage. Conclusively, this study provides a foundation for optimizing surgical strategies and improving patient outcomes in this high-risk population.
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
Awards: G1632724801, G5321960718, G7144161934
OpenAlex ID: W7125284425
