Major abdominal wall reconstruction (AWR) for large ventral hernias is among the most physiologically demanding procedures performed in general surgery. These patients often have a history of multiple prior abdominal operations, chronically altered abdominal wall mechanics and significant loss of domain. Reduction of visceral contents and abdominal wall reconstruction frequently require high-tension closure, resulting in an abrupt increase in intra-abdominal pressure (IAP) that impairs diaphragmatic excursion, reduces splanchnic perfusion, causes renal venous congestion and induces global physiologic stress. Consequently, these patients face a high risk of postoperative complications including respiratory failure, renal dysfunction, and prolonged intensive care unit (ICU) stays.
A critical gap in AWR research is the lack of characterization of the biologic inflammatory and cytokine responses associated with high-tension abdominal wall closure. This gap stands in contrast to robust evidence from the trauma and critical care literature demonstrating that cytokine activation correlates with injury severity and contributes to organ dysfunction and postoperative morbidity.
Defining the inflammatory and cytokine signaling pathways activated during high-tension closure would provide a framework to inform operative planning and perioperative management, particularly in patients with significant comorbidities who may be less tolerant to postoperative physiologic stress. These insights would enable validation of current techniques and establish the foundation for future interventional trials targeting inflammatory pathways to improve postoperative outcomes. The Digestive Health Institute at Northwestern University is uniquely positioned to support this translational research, bridging surgical physiology, inflammation, and patient outcomes.
The investigators hypothesize that:
1. Major abdominal wall reconstruction induces a trauma-like systemic inflammatory response characterized by elevations in GM-CSF, IFN-Gamma, IL-1, IL-2, IL-5, IL-6, IL-8, and TNF-alpha with a concomitant decrease in the anti-inflammatory cytokines, IL-4 and IL-10.
2. Increased intra-abdominal pressure (IAP) following high-tension closure amplifies cytokine activation and is associated with early postoperative organ dysfunction and increased postoperative complications.
