History and admission findings: A 71-year-old patient had been referred to our hospital with the diagnosis, made by angio-computed tomography (CTA), of a covered ruptured abdominal aortic aneurysm (AAA) resulting in an aortocaval fistula (ACF).Investigations: The physical examination revealed macrohematuria and high-output heart failure with increasing circulatory insufficiency.Diagnosis, treatment and course: An open endovascular procedure was not possible because the AAA had extended into both internal iliac arteries. A bifurcated prosthesis connecting to both femoral arteries was then successfully implanted and the infrahepatic aortocaval fistula closed by a patch through the AAA. Ischemic colitis, diagnosed on postoperative day 2 (POD 2), was successfully treated with antibiotics. CTA, done on POD 5, revealed a small residual ACF, filling retrogradely from the right external iliac artery via the surgically closed aneurysmal sack. Closure of the residual ACF was achieved with an Amplatz occluder inserted into the right external iliac artery, introduced percutaneously via the right femoral artery. The postoperative course was uneventful and the patient discharged on POD 13.Conclusion: The coincidence of AAA and ACF is rare. However, the morbidity and mortality are high and require early diagnosis and immediate treatment.

Bei allen therapeutischen Überlegungen sollte zugrunde gelegt werden, dass, unabhängig von der Lokalisation (terminales Ileum, ileokolisch, Kolon) und vom Verhalten (inflammatorisch, fibrosierend-stenosierend, fistulierend), der Morbus Crohn weder durch eine medikamentöse noch durch eine chirurgische Therapie derzeit heilbar ist. Die chirurgische Therapie hat unter der Voraussetzung, dass sie entsprechend sensibel und Darm schonend zur Vermeidung eines Kurzdarmsyndroms durchgeführt wird, nach wie vor einen hohen Stellenwert. Unterschieden werden sollte zwischen reversiblen entzündlichen Stenosen bei primär inflammatorischen Verlaufsformen, die einer konservativen Therapie gut zugänglich sind, und narbigen Stenosen bei primär eher fribrosierenden Verlaufsformen, die frühzeitig einer chirurgischen Intervention bedürfen. Bei Patienten mit fistulierenden und entsprechend komplizierten Verlaufsformen besteht die Notwendigkeit zur engen interdisziplinären Zusammenarbeit, um individuell den richtigen Operationszeitpunkt für den jeweiligen Patienten festzulegen. Auch wenn die Therapie des Morbus Crohn primär eine medikamentöse ist, benötigen fast 75% aller Morbus-Crohn-Patienten innerhalb der ersten 3 Jahre nach Diagnosestellung und 80–90% während ihres Lebens eine entsprechende chirurgischen Therapie. Dementsprechend sollte Ziel der interdisziplinären Zusammenarbeit sein, den Operationszeitpunkt so zu wählen, dass Morbus-Crohn-bedingte Komplikationen, eine im Krankheitsverlauf zu erwartende Reduzierung des Allgemeinzustands, eine potentiell mögliche maligne Entartung ebenso wie relevante medikationsbedingte Nebenwirkungen vermieden werden.

Die Endothelin-vermittelte Leukozyten-Endothelzell-Interaktion folgt einer strengen Dosiswirkungsbeziehung, wobei überraschenderweise keine Unterschiede zwischen den drei Endothelinen detektierbar sind. Die Endothelin-stimulierte Endothelzellaktivierung, gemessen anhand der Adhärenz von unspezifischen Latexpartikeln, korreliert nicht mit dieser Dosiswirkungsbeziehung. Dies gibt Hinweis, dass die Endothelin-induzierte Leukozytenadhärenz nicht ausschließlich durch das Ausmaß der Endothelzellaktivierung bestimmt wird.

Der Ileuskrankheit liegt eine manifeste Störung der Darmpassage zugrunde, deren Ursachen vielfältig sind. Diese führen über verschiedene pathophysiologische Mechanismen wie Distension des Darmlumens, Störungen der Mikrozirkulation und Elektrolytverschiebungen zur Dekompensation lebenswichtiger Organsysteme. Aus diesen pathophysiologischen Veränderungen ergeben sich gegebenenfalls nicht operative Therapieoptionen, vorausgesetzt es besteht kein das Darmlumen obstruierendes, mechanisches Hindernis. Der Ersatz von Wasser- und Elektrolytmengen sind neben der mechanischen Dekompression mittels entlastenden Magen- oder Darmsonden von entscheidender Bedeutung für den Erfolg der konservativen Therapie.

Intestinal obstruction may be mechanical or non-mechanical (adynamic ileus). Adhesions and external hernias are the most common causes of obstruction in small intestine, whereas carcinoma, sigmoid diverticulitis, and volvulus are the most common causes in large intestine obstruction. Distension of the intestine caused by gas and fluid accumulation in the obstructed segment is the key pathophysiological mechanism initiating ileus with subsequent multiorgan failure and death. Surgery should always be undertaken if complete obstruction or strangulation is suggested and ileus is established. Before operation, the fluid and electrolyte balance should be restored and decompression instituted by means of a nasogastric tube. Delaying the operation because of improvement in patient well-being during resuscitation is only justified in those suffering from large intestine obstruction due to colorectal carcinoma. Purely nonoperative treatment is safe only in the presence of incomplete obstruction and best utilized in patients with postoperative adynamic ileus or repeated episodes of partial obstruction.

Introduction: Endothelin plays a key role in mediating pancreatitis-associated inflammation. The inflammatory response is triggered by the activation of microvascular endothelial cells and their interaction with stimulated polymorphonuclear leukocytes. It is still unclear, however, which endothelin receptor (ETA, ETB) mediates the pancreatitis-associated inflammatory response. Using the rat model of sodium-taurocholate-induced pancreatitis and intravital microscopy, we therefore studied whether selective inhibition of ETA or ETB receptor function affects pancreatitis-associated leukocyte-adhesion and endothelial cell activation. Methods: For intravital microscopy 24 male Sprague Dawley rats were anesthetized with sodium pentobarbital (50 mg/kg i. p.) followed by laparotomy and exterioration of the pancreas. After inhibition of either the ETA receptor (BQ 123, n = 8) or the ETB receptor (BQ 788, n = 8) and creating of a sodium-taurocholate (4%)-induced pancreatitis, leukocyte-adhesion and endothelial cell activation were investigated using intravital microscopy, rodamin 6G-stained leukocytes and fluorescent-stained latex particles (diameter: 1 μm). Animals which did not receive pre-treatment by ET receptor-antagonists prior to pancreatitis induction served as controls (n = 8). Data are given as means ± SEM; statistics included ANOVA and post-hoc Student-New-man-Keuls test. Results: Induction of an acute experimental pancreatitis caused a significant increase in leukocyte adherence from 93 ± 19 sticker/mm2 venular endothelial surface at baseline to 621 ± 84 sticker/mm2 at 2 h after induction of pancreatitis. This was associated with an endothelial cell activa-tion of 18 ± 0.4 beads/mm2. Inhibition of the ETA receptor (BQ 123) reduced leukocyte adhesion (225 ± 39 sticker/mm2, p < 0.05) and endothelial cell activation (11 ± 0.3 beads/mm2, p < 0.05). In contrast, selective inhibition of the ETB receptor (BQ 788) did neither affect leukocyte adhesion (615 ± 112 sticker/mm2) nor endothelial cell activation (26 ± 5.5 beads/mm2) when compared to controls. Conclusion: These results indicate that the pancreatits-associated endothelial cell activation and leukocyte-endothelial adhesion is mediated by the ETA but not the ETB receptor.

PURPOSE: Short-term benefits have been demonstrated for laparoscopic-assisted colectomy. However, minimally invasive surgery is still in an evolutionary phase. In demonstrating that robotic devices also are useful in laparoscopic colonie surgery, it is fundamental to prove that a single surgeon can perform almost the entire operation on his own. METHODS: A single surgeon performed forty-one, laparoscopic-assisted, colorectal resections with the assistance of a robotic device (Automated Endoscopie System for Optimal Positioning, Computer MotionTM) maneuvering the laparoscope. A surgical assistant was included only for the open part of the operation. Main outcome measures were conversion rate, total operating time, and percentage of assistance by a second surgeon. RESULTS: There were no intraoperative complications, one case of conversion to open surgery, and three postoperative complications. The total operating time ranged from 126 to 252 minutes. A single surgeon with the assistance of a robotic device was able to perform approximately 70 percent of an ileocecal resection, 70 percent of a right hemicolectomy, 80 percent of a sigmoid resection, and 85 percent of a anterior rectal resection without further help of a surgeon. CONCLUSIONS: A single surgeon with the assistance of a computerized robotic system can complete at least two-thirds of a laparoscopic-assisted, colorectal resection on his own. The use of a robotic device in laparoscopic-assisted, colonie surgery is safe, efficient, and feasible, and will proven even more so in future. This also will result in a patient-driven demand for high-standard, minimally invasive surgery.

Background: The magnitude of surgical trauma after laparoscopic and open colonic resection was evaluated by examining postoperative serum values of interleukin-6 (IL-6), IL-10, C-reactive protein (CRP), and granulocyte elastase (GE) for further evidence of the benefit realized with minimally invasive approaches in colonic surgery. Methods: Altogether, 42 patients with Crohn's disease (n = 20) or colon carcinomas/adenomas (n = 22) were matched by age, gender, body mass index (BMI), and Crohn's Disease Activity Index for either a laparoscopic (n = 21) or an open colonic resection (n = 21). In both groups the postoperative serum levels of IL-6, IL-10, C-RP, and granulocyte elastase were determined, as indicators of surgical stress. Results: Laparoscopic and open colonic resection caused a significant increase in serum IL-6, IL-10, CRP, and granulocyle elastase levels. The comparison between laparoscopic and open colonic resections, however, showed significantly lower serum IL-6, IL-10, CRP, and granulocyte elastase levels after laparoscopic colonic resection, which was most evident for IL-6 and granulocyte elastase. Conclusions: Our study demonstrated that IL-6 and granulocyte elastase may be appropriated particularly to monitor surgical stress. By using these parameters, we found a significant reduction in surgical trauma after laparoscopic surgery, was compared with the open procedure. This supports the clinical findings of a clear benefit for patients undergoing laparoscopic colonic surgery.

The role of endothelin (ET)A and ETB receptor function in experimental pancreatitis is still not fully understood. Using a rat model of sodium taurocholate-induced pancreatitis and intravital microscopy, we therefore studied whether selective inhibition of ETA receptor function or combined ETA and ETB receptor blockade affects the development of pancreatitis-associated microcirculatory failure, inflammation, and parenchymal injury. Pretreatment with 10 mg/kg body wt of a combined ETA/B receptor antagonist, which is thought to mediate a simultaneous inhibition of both receptors, did not attenuate the pancreatitis-induced microcirculatory failure, inflammatory response, and parenchymal tissue injury. In contrast, pretreatment with a low concentration of the combined ETA/B receptor antagonist (4 mg/kg body wt), which predominantly inhibits the ETA receptor, revealed an improvement of some microcirculatory disorders and a significant attenuation of leukocyte recruitment and tissue injury. Furthermore, pretreatment with a selective ETA receptor antagonist (1 microg/kg body wt) almost abolished pancreatitis-associated capillary constriction, restored functional capillary density, and, consequently, improved overall nutritive perfusion. Importantly, the maintenance of an appropriate microcirculation by selective ETA receptor inhibition was accompanied by a significant attenuation of the inflammation-associated leukocytic response and by a marked reduction of parenchymal injury. Thus our study indicates that pancreatitis-associated development of microcirculatory failure, inflammation, and parenchymal injury is caused by ETs coupling onto the ETA receptor, which therefore may represent a promising target for novel strategies in the treatment of pancreatitis.

The differential effects of endothelin-1, -2, and -3 (ET-1, ET-2, and ET-3) on pancreatic microcirculation, pancreatic tissue integrity, and an initial inflammatory response, which are three distinct characteristics of acute necrotizing pancreatitis, were investigated in a dose-dependent manner in rats using in vivo microscopy. Red blood cell (RBC) velocity and functional capillary density (FCD) were estimated after topical superfusion of the pancreas with ET-1, ET-2, and ET-3 (100, 10, 1 pmol), revealing that ET-1 (100, 10, 1 pmol) or high ET-2 (100 pmol) and ET-3 (100 pmol) cause a dose-related deterioration of exocrine nutritive pancreatic blood flow. Analysis of pancreatic exocrine tissue damage employing the Spormann score displayed that the ET-mediated microcirculatory impairment was paralleled by dose-dependent tissue damage, which was significant compared to the control group (topical superfusion with 1 ml, saline solution 0.9%). Estimation of pancreatic postcapillary leukocyte accumulation by histomorphologically counting choracetate esterase (CAE) stained leukocytes in 50 high-power fields per animal demonstrated a significant increase in postcapillary accumulation of white blood cells, after topical administration of ET-1, ET-2, and ET-3 compared to controls. In contrast to ET-caused effects on microcirculation and tissue impairment, quantitative analysis of postcapillary leukocyte accumulation revealed the most pronounced effect after ET-2 administration but not after ET-1 administration. This demonstrates that ET-1, ET-2, and ET-3 are all able to mediate microcirculatory impairment, tissue damage, and inflammation. However, ET-3-induced damaging effects are less pronounced, while ET-1 most severely alters microcirculation and ET-2 preferentially induces leukocyte-dependent inflammation.

Temporary obliteration of the pancreatic duct has been suggested to be beneficial in chronic pancreatitis, segmental pancreatic transplantation, and following Roux-Y pancreaticojejunostomy. Little is known, however, as to whether obliteration of the duct alters exocrine pancreatic physiology. Therefore we studied in male inbred Lewis rats the immediate effects of Ethibloc-induced duct obliteration (Ethibloc: Ethicon, Norderstedt, Germany) on pancreatic microcirculation, inflammation, and tissue injury ( n = 8), and compared these effects with those caused by experimental pancreatitis (4% sodium taurocholate; n = 8). Animals receiving an intraductal infusion of saline served as controls ( n = 8). Duct occlusion with Ethibloc resulted in a marked decrease ( p < 0.05) in capillary red blood cell (RBC) velocity and functional capillary density (FCD) to 88 ± 39 μm/s (baseline 716 ± 40 μm/s) and 72 ± 33 cm −1 (baseline 493 ± 21 cm −1 ), respectively, which was even more pronounced when compared with that observed in experimental pancreatitis (333 ± 62 μm/s and 195 ± 44 cm −1 , respectively). In parallel, the manifestation of tissue damage was found to be more severe after Ethibloc; and chloracetate esterase staining showed a larger number of infiltrating leukocytes [555 ± 86/high power field (HPF) versus pancreatitis: 160 ± 12/HPF; p < 0.05). We conclude that intraductal application of Ethibloc induces significant microcirculatory failure and a marked inflammatory response, which are even more pronounced when compared with the changes observed with experimental pancreatitis. Based on these results and the fact that there is no direct proof for a benefit of temporary duct occlusion by Ethibloc, it is proposed that the procedure be reevaluated for its use in pancreatic surgery.

During the past decade, a considerable number of experimental studies have confirmed the hypothesis that microcirculatory derangements play a pivotal role in the pathogenesis of acute pancreatitis, including the process of conversion from edematous to necrotizing injury. Predominant microcirculatory disorders are nutritive capillary perfusion failure, with the consequence of prolonged focal hypoxia or anoxia, and inflammation-associated microvascular leukocyte recruitment, CD11b- and intercellular adhesion molecule (ICAM)-1-mediated leukocyte-endothelial cell interaction and loss of endothelial integrity, which may result in both edema formation and necrosis. A variety of proinflammatory mediators, such as oxygen radicals, leukotrienes, platelet-activating factor, and interleukins, but also bradykinin and endothelins, seem to be involved in triggering the manifestations of these microcirculatory disorders. In contrast, the anti-inflammatory interleukin-10, as well as nitric oxide, are thought to be capable of protecting from these pancreatitis-associated microvascular injuries. This knowledge may be encouraging for the development of novel therapeutic strategies, aiming at the attenuation of microcirculatory disorders, and, thus, preventing tissue injury in acute pancreatitis.

Using in vivo microscopy red blood cell (RBC) velocities, functional capillary density (FCD) and capillary diameters were estimated after inducing acute pancreatitis by intraductal infusion of sodium taurocholate (0.8 ml; 4%) or after topical superfusion of the pancreas with ET-1 (100 pmol). Sodium taurocholate mediated a significant decrease in RBC velocities between 50 and 70%, transient decrease in capillary diameters by 10%, and a sustained decrease in FCD between 60 and 70% paralleled by a dramatic heterogeneity in blood flow. Topical superfusion of the exteriorized pancreas with ET-1 caused a significant decrease in RBC velocities between 65 and 75%, a sustained decrease in capillary diameters by 10%, and a decrease in FCD by 45% accompanied by an increase in flow heterogeneity. Following sodium taurocholate infusion pancreas histology revealed a severe edema and sublobular acinar cell necrosis, while topical ET-1 application displayed a severe edema of the pancreas with focal acinar cell necrosis. Thus, ET-1 mediated a deterioration of the pancreatic microcirculation, which is similar to the microcirculatory failure found in sodium taurocholate-induced experimental pancreatitis and was associated with focal acinar cell necrosis. We are thus inclined to hypothesize that endothelin released by injured endothelial cells during acute biliary pancreatitis promotes microcirculatory failure and ischemia in acute pancreatitis, eventually leading to acinar cell necrosis.