Intestinal stasis followed by mucosal barrier breakdown and the generation of locally produced cytokines has been proposed as the cause of systemic infection and multiple organ failure following hemorrhagic shock. The aim of this study was to investigate the underlying mechanisms of impaired intestinal muscle function leading to ileus following hemorrhagic shock. Rats were subjected to severe hemorrhagic shock (mean arterial pressure 40 mm Hg) followed by resuscitation and were killed early at 4 h or late at 24 h. Other groups consisted of control and sham animals. Intercellular adhesion molecule (ICAM-1) mRNA levels were significantly elevated in the muscularis but not in the mucosa using the semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR). There was a marked infiltration of neutrophils into the muscularis early and late after shock. Furthermore, smooth muscle contractility in response to bethanechol was significantly decreased, being more pronounced in the early group. Immunohistochemistry revealed signal for ICAM-1 in the muscularis microvasculature and on infiltrating cells. These results suggest that the expression of ICAM-1 within the muscularis vasculature after hemorrhagic shock promotes the local recruitment of leukocytes and that this inflammatory response is accompanied by a subsequent impairment of intestinal contractility.

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Short bowel syndrome, with a newly estimated prevalence of 34/million inhabitants is not a very rare medical condition in Germany. The interdisciplinary approach needed for optimal care for SBS patients would be greatly facilitated by a central registry.

Pancreatic fistulas and related complications represent the most common indications for revisions, but can usually be controlled by interventional procedures. In contrast to secondary surgery, interventional revisions do not significantly increase the length of hospital stay or mortality. There was no benefit of any certain closure technique of the pancreatic remnant.

Postoperative ileus (POI) is defined as a transient episode of impaired gastrointestinal motility after abdominal surgery, which prevents effective transit of intestinal contents or tolerance of oral intake. This frequent postoperative complication is accompanied by a considerable increase in morbidity and hospitalisation costs. The aetiology of POI is multifactorial. Besides a suppression of peristalsis by inhibitory neuronal signalling and administration of opioids, particularly in the prolonged form, immunological processes play an important role. After surgical trauma, resident macrophages of the muscularis externa (ME) are activated leading to the liberation of proinflammatory mediators and a spreading of the inflammation along the entire gastrointestinal tract. To date, no prophylaxis or evidence-based single approach exists to treat POI. Since none of the current treatment approaches (i.e., prokinetic drug treatment) has provided a benefit in randomised trials, immunoregulatory interventions appear to be more promising in POI prevention or treatment. The present contribution gives an overview of immunological mechanisms leading to POI focusing on current and future therapeutic and prophylactic approaches.