[Single-port access cholecystectomy is a safe alternative to conventional laparoscopic cholecystectomy: a retrospective comparison of single-port access versus standard laparoscopic cholecystectomy]. / Single-Port-Access-Cholezystektomie als sichere Alternative zum 4-Port-Vorgehen: Ein retrospektiver Vergleich.

PURPOSE: As laparoscopic surgery develops, one current goal is the reduction of scarring and operative trauma to a minimum. Single-port access surgery (SPA) uses a single small incision hidden in the umbilicus. This report describes our experiences with 69 SPA cholecystectomies compared to the conventional laparoscopic approach. METHODS: Within two years 69 SPA cholecystectomies were performed. Data including demographic distribution, incision to closure time, duration of the postoperative hospital stay, rates of intraoperative and postoperative complications, and conversion rates were collected retrospectively. Data for a matched control group treated by standard laparoscopic cholecystectomy were gathered within the same time frame and then compared. RESULTS: There were no significant differences in the rates of intraoperative or postoperative complications in the SPA group when compared to the standard laparoscopy group. The incision-to-closure time strongly depended on the surgeon but did not depend on the method. The duration of postoperative hospital stay was slightly decreased in the SPA group. However, this effect was statistically not significant. CONCLUSIONS: For selected patient groups, SPA cholecystectomy is on par with the conventional laparoscopic method. The cosmetic advantage that it offers does not come at the cost of any loss of safety.

Surgical trauma and postoperative immune dysfunction.

BACKGROUND: In postoperative sepsis, mortality is increased due to the surgically induced immune dysfunction. Further causes of this traumatic effect on the immune system include burn injuries and polytrauma, as well as endogenous traumata like stroke. Several animal models have been defined to analyse the characteristics of trauma-induced immune suppression. This article will correlate our results from animal studies and clinical observations with the recent literature on postoperative immune suppression. METHODS: The previously described model of surgically induced immune dysfunction (SID) was performed in mice by laparotomy and manipulation of the small intestine in the antegrade direction. Blood samples were collected 6 and 72 h following SID to analyse the white blood cell count and corticosterone levels. To assess the postoperative immune status in humans, we analysed expression of HLA-DR on monocytes of 118 patients by flow cytometry prior to and 24, 48 and 72 h after surgery. RESULTS: The postoperative immune suppression in our SID model is characterised by lymphocytopenia and significantly increased corticosterone levels in mice dependent on the degree of surgical trauma. This is comparable to the postoperative situation in humans: major and especially long-lasting surgery results in a significantly reduced expression of HLA-DR on circulating monocytes. Previous studies describe a similar situation following burn injury and endogenous trauma, i.e. stroke. CONCLUSIONS: We suggest the completion of our previously published sepsis classification due to the immune status at the onset of sepsis: type A as the spontaneously acquired sepsis and type B as sepsis in trauma-induced pre-existing immune suppression.

Postoperative immune suppression in visceral surgery: characterisation of an intestinal mouse model.

BACKGROUND: Postoperatively acquired immune dysfunction is associated with a higher mortality rate in case of septic complications. As details of this severe clinical problem are still unknown, animal models are essential to characterise the mechanisms involved. METHODS: Mice were laparotomised and the small intestine was pressed smoothly in antegrade direction. For extension of trauma, the intestine was manipulated three times consecutively. Following this, the ex vivo cytokine release of splenocytes was determined. The degree of surgical trauma was analysed by detection of HMGB1 and IL-6 in serum and by neutrophil staining in the muscularis mucosae. RESULTS: We adapted the previously described animal model of intestinal manipulation to provide a model of surgically induced immune dysfunction. Following intestinal manipulation, the mice showed elevated serum levels of HMGB1 and IL-6 and increased infiltration of granulocytes into the muscularis mucosae. Ex vivo cytokine release by splenocytes was suppressed in the postoperative period. The degree of suppression correlated with the extent of surgical trauma. CONCLUSIONS: In this study, we describe a surgically induced immune dysfunction animal model, in which a significant surgical trauma is followed by an immune dysfunction. This model may be ideal for the characterisation of the postoperative immune dysfunction syndrome.

Stimulation of TLR7 prior to polymicrobial sepsis improves the immune control of the inflammatory response in adult mice.

OBJECTIVE: The role of Toll-like receptor 7 (TLR7), so far regarded as a receptor for viral RNA, was evaluated in a murine sepsis model. MATERIAL: We used the colon ascendens stent peritonitis model (CASP) in female C57B/6 mice. R-848 (1.5 µg/g body weight) was injected intravenously prior to sepsis induction. METHODS: We determined levels of cytokines by CBA detection kit. Different cell populations were isolated from the spleen by magnetic cell separation and the expression of TLR7 was visualized by immunofluorescence staining. Bacterial load of organs was quantified by incubating suspensions on agar in colony forming units. RESULTS: R-848 application per se led to elevated cytokine levels in serum, spleen and peritoneal cavity. Expression of TLR7 on splenocytes was upregulated following CASP. Bacterial clearance in polymicrobial sepsis was significantly increased in spleen and peritoneum of mice pre-treated with the TLR7-agonist. Cytokine release was regulated in the peritoneum and spleen. Furthermore, apoptosis in thymus and spleen during polymicrobial sepsis was significantly decreased following TLR7 agonist application. CONCLUSIONS: TLR7 seems to be essential for pathogen defence not only in viral but also in bacterial infections. Pharmacological stimulation of this receptor prior to induction of sepsis improves the host's capacity to cope with pathogens.

[Atypical vascular supply from the coeliac trunk. Recurrent bleeding from a duodenal ulcer]. / Atypische Gefässversorgung aus dem Truncus coeliacus. Rezidivblutung aus einem Ulcus duodeni.

Hemorrhagic duodenal ulcers should primarily be controlled by endoscopy. In cases of recurrent bleeding or if bleeding cannot be controlled endoscopically, open surgery is the gold standard. Rarely, atypical origin of arteries or additional atypical arteries may lead to further unexpected hemorrhagic recurrences and angiography with surgical intervention is the treatment of choice. In this article a rare case of an atypical visceral artery connecting the coeliac trunk and the gastroduodenal artery leading to recurrent bleeding from a duodenal ulcer is presented.