Peritonitis from perforated peptic ulcer and immune response

Elevated intra-abdominal pressure during the laparoscopy may promote bacteremia, endotoxemia, and systemic inflammatory response. In patients with generalized peritonitis from perforated peptic ulcer (PPU), we sought to compare acute phase response, immunologic status, and bacterial translocation from laparoscopic and open approach.

From July 2005 to September 2011, 115 consecutive patients underwent peptic ulcer repair for PPU: 58 cases laparoscopic peptic ulcer repair (LR) and 57 cases open peptic ulcer repair (OR). Bacteremia, endotoxemia, white blood cells population, human leukocyte antigen-DR (HLA-DR), neutrophil-elastase, interleukin-1 and 6 (IL-1 and IL-6), and C-reactive protein (CRP) were investigated.

Patients characteristics and grade of peritoneal contamination were similar in the two groups. One hour after intervention, bacteremia was significantly higher in the "open" group than in the laparoscopic group (p < .001). A significantly higher concentration of systemic endotoxin was detected intraoperatively in the "open" group of patients in comparison to the laparoscopic group (p < .0001). Laparotomy caused a significant increase in neutrophil concentration, neutrophil-elastase, IL-1 and IL-6, CRP, and decrease of HLA-DR. We recorded six cases (10.3%) of intra-abdominal abscess in the "open" group and one (1.7%) in laparoscopic group (p < .001).

OR, in case of peritonitis after PPU, increased the incidence of bacteremia, endotoxemia, and systemic inflammation compared with LR. Early enhanced postoperative systemic inflammation may cause lower transient immunologic defense after laparotomy (decrease of HLA-DR), leading to enhanced sepsis in these patients.