[Multimodal approach in coincidence of covered ruptured abdominal aortic aneurysm and aortocaval fistula]. / Multimodales Vorgehen bei einem gedeckt rupturierten Bauchaortenaneurysma mit aortocavaler Fistel.

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.

[Ileus disease]. / Ileuskrankheit.

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.

Single-surgeon surgery in laparoscopic colonic resection.

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 colonic 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 Endoscopic System for Optimal Positioning, Computer Motion) 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, colonic surgery is safe, efficient, and feasible, and will prove even more so in future. This also will result in a patient-driven demand for high-standard, minimally invasive surgery.

ETA and ETB receptor function in pancreatitis-associated microcirculatory failure, inflammation, and parenchymal injury.

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.

Comparison of surgical stress between laparoscopic and open colonic resections.

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 granulocyte 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.

Microcirculatory derangements in acute pancreatitis.

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.

Differential effects of ET-1, ET-2, and ET-3 on pancreatic microcirculation, tissue integrity, and inflammation.

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 pancreatic duct occlusion by ethibloc: cause of microcirculatory shutdown, acute inflammation, and pancreas necrosis.

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 microm/s (baseline 716 +/- 40 microm/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 microm/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.

ET-1 induces pancreatitis-like microvascular deterioration and acinar cell injury.

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.

Somatostatin attenuates microcirculatory impairment in acute sodium taurocholate-induced pancreatitis.

Using in vivo microscopy, red blood cell (RBC) velocities, functional capillary density (FCD), and overall changes in capillary blood flow (PI) were estimated following intraductal infusion of sodium taurocholate (0.8 ml; 4%) alone or in combination with systemic administration of somstostatin (single bolus SMS 100 microg/100 g body wt). Sodium taurocholate mediated a significant transient decrease in RBC velocities and a sustained decrease in FCD, which were paralleled by dramatic flow heterogeneity. Therefore, a significant reduction in overall capillary blood flow was calculated. Additional SMS treatment reduced microcirculatory impairment as expressed by reduction of blood flow heterogeneity, a less rarified functional capillary density, and a recovery of RBC velocities and acinar capillary overall perfusion to control values. As a result of this microcirculatory improvement, pancreas histology revealed slightly less severe tissue damage compared to the non-SMS-treated pancreatitis group. These findings demonstrate that exogenous SMS infusion can improve microcirculatory failure in acute biliary pancreatitis, which should have a beneficial effect on the course of the disease.

Effects of somatostatin (SMS) on pancreatic microcirculation.

The effect of bolus infusion of increasing somatostatin (SMS) concentrations (1, 10, 100, 200 micrograms/100 g body wt) on pancreatic microcirculation and pancreatic tissue PO2 were investigated by using in vivo epifluorescence microscopy and a polarographic PO2 measurement technique. Additionally, the microperfusion of the pancreas, liver, spleen, stomach, and duodenum was measured by a laser Doppler device. Bolus infusion of SMS caused a significant, transient, and dose-dependent decrease in pancreatic capillary RBC velocities (to 50% of baseline) and acinar capillary overall perfusion (to 20% of baseline), which was not caused by a macrocirculatory depression. This pronounced decrease in microperfusion was not paralleled by a decline in tissue PO2. Laser Doppler measurements revealed that pancreatic and gastric microperfusion were reduced only at maximal SMS concentrations, considering that microperfusion of the liver, spleen, and duodenum was not altered. Therefore, we found further evidence that circulatory adjustment might occur during SMS inhibited secretory activity of the exocrine pancreas.

Acute pancreatitis in rats: effects of sodium taurocholate, CCK-8, and Sec on pancreatic microcirculation.

With use of in vivo microscopy, pancreatic duct permeability, red blood cell (RBC) velocities, functional capillary density (FCD), and overall changes in capillary blood flow (perfusion index) were estimated after intraductal infusion of sodium taurocholate (0.8 ml, 4%) alone or in combination with systemic administration of cholecystokinin (CCK, 0.3 microg/100 g body wt) or secretin (Sec, 10 microg/100 g body wt). Sodium taurocholate mediated a significant increase in pancreatic duct and capillary permeability within 105 +/- 26 s followed by a transient decrease in RBC velocities and a sustained decrease in FCD, which were paralleled by dramatic flow heterogeneity. Therefore, a significant reduction in overall capillary blood flow was calculated. CCK stimulation aggravated the microcirculatory failure due to a decrease in RBC velocities, which was accompanied by an increase in acinar cellular necrosis. Sec stimulation attenuated microcirculatory failure due to a more moderate reduction of FCD. The enhanced pancreatic duct and capillary permeability, which enables free diffusion of pancreatic digestive enzymes into the parenchyma, is the initiating event in acute biliary pancreatitis, causing microcirculatory failure and tissue damage. The microcirculatory changes are secondary and a propagating factor for the development of acini necrosis. Stimulation with CCK worsened the course of acute biliary pancreatitis.

Comparative effects of secretin (SEC) and cholecystokinin-octapeptide (CCK-8) on pancreatic microcirculation.

Using epifluorescent microscopy, we investigated the dynamic changes in pancreatic microcirculation in vivo after bolus administration of secretin (SEC) (0.1-10.0 micrograms/100 g body wt) and cholecystokinin-octapeptide (CCK-8) (0.005-1.2 micrograms/100 g body wt) in pentobarbital-anesthetized rats. Pancreatic capillary red cell velocity as a monitor for pancreatic capillary blood flow was measured in 1-min intervals from 2 min prior to 8 min following bolus infusion of SEC or CCK-8. Physiological concentrations of SEC did not increase pancreatic capillary blood flow. However, pharmacological SEC concentrations induced a dose-dependent increase in pancreatic capillary blood flow (to 162 +/- 19% of baseline; P < 0.05), due to an increase in blood flow velocity (to 153 +/- 18% of baseline; P < 0.05). In contrast, bolus administration of physiological CCK-8 concentrations, which have been proven to stimulate enzyme secretion, induced a transient and dose-dependent increase in pancreatic capillary blood flow (to 235 +/- 24% of baseline; P < 0.05), due to an increase in blood flow velocity (to 184 +/- 13% of baseline; P < 0.05) and capillary diameters (+0.63 +/- 0.15 micron; P < 0.05).

[Experimental approach to left laparoscopic pancreas resection preserving the spleen]. / Experimenteller Ansatz zur laparoskopischen Pankreaslinksresektion unter Erhalt der Milz.

The pancreas has been excluded from laparoscopic surgery ever since. The technical possibilities of laparoscopic left resection of the pancreas in pigs are examined in this study. Mobilization of the left pancreatic segment up to the confluence area (splenic vein and upper mesenteric vein) was possible preserving the spleen. Sectioning of the organ was performed by ultrasound dissector and selective clipping of the pancreatic duct in 4 animals, in 2 animals this was achieved by Endo-GIA. The size of resected segments was 10-15 cm in length, 2-4 cm in width and the segments weighed 30 gr. Laparoscopic left resection of the pancreas with preservation of the spleen is technically possible in pigs. Postoperative complications have to be further examined in survival studies.

[Technique and quality of laparoscopic hand-sewn intestinal anastomoses in an experimental procedure]. / Technik und Qualität laparoskopisch handgenähter Darmanastomosen im Experiment.

In conventional surgery running suture of all intestine layers is used commonly. Therefore we have tested the following manual running suture technics for laparoscopic surgery using animal experiments. 1. Turnover technic: suture of front and back-wall from outside by using holding sutures. 2. Non-turnover-technic: special holding sutures to fix the back-wall and sewing from the inside followed by the front-wall from outside. 3. Clamp-technic: By using two special parallel closing clamps (Endo-Gauge) with a suture from inside and outside. The ends of the anastomosis are well fixed without additional suture. All animals (n = 15) survived without complications, without leakage of the anastomosis and only one third developed intraabdominal fusions. The main difference was in time performing the anastomosis: 64 min. for the turnover technic, 52 min. for the non-turnover technic and only 25 min for the clamp technic without holding sutures. According to this results, we start to design a new bowel-clamp for sewing laparoscopic anastomosis. Therefore it is possible to perform a laparoscopic manual running suture in a reasonable amount of time. Furthermore the laparoscopic manual suture is a good alternative to the stapler technic because it is much less expensive and leaves no foreign materials.

Coagulation inhibitors in pulmonary cancer patients.

Pulmonary cancer patients are known to have an elevated risk to suffer from thromboembolic complications. Because hereditary deficiencies of coagulation inhibitors antithrombin III, protein C and protein S are known to cause thromboembolic events it was the aim of our study to search for acquired alterations of these proteins in pulmonary cancer patients. We could demonstrate antithrombin III and protein C to be within the normal range in patients suffering from pulmonary carcinoma. In contrast, in patients suffering from metastatic pulmonary carcinoma bound protein S was increased, while free protein S was significantly reduced. In some patients the decrease of free protein S was comparable to the diminution observed in hereditary protein S deficient patients. A high positive correlation was observed between C4b-binding protein and bound protein S, indicating C4b-binding protein to be a regulatory protein for the shift from free and anticoagulatory active to bound and anticoagulatory inactive protein S. In conclusion, the decrease of free protein S is one source for thromboembolic complications in pulmonary cancer patients. For interpretation of altered free protein S levels it is useful to measure C4b-binding protein.

PGE2 regulates cholecystokinin-octapeptide (CCK-8)-stimulated Cl- conductance in isolated zymogen granules from rat pancreas.

In this study we have examined the effects of prostaglandin E2 (PGE2), the cyclooxygenase inhibitor, indomethacin, and a protein kinase A inhibitor (PKA-I) on the Cl- conductance in isolated zymogen granules (ZG) from cholecystokinin octapeptide (CCK-8) pre-stimulated pancreatic acini. The Cl- conductance in isolated ZG from CCK-8 pre-stimulated rat pancreatic acini increases with increasing CCK-8 concentrations and decreases at supramaximal CCK-8 concentrations. The basal and CCK-8-stimulated Cl- conductance in ZG is inhibited by pretreatment of acini with PGE2 (10(-6) M). This PGE2-induced inhibition is abolished in the presence of PKA-I (20 U/ml). Furthermore, pretreatment of acini with indomethacin (10(-5) M) or PKA-I (20 U/ml) abolishes the decrease in the CL- conductance at supramaximal CCK-8 concentrations (10(-9) M). We conclude that the inhibition of the CL- conductance in isolated ZG at high CCK-8 concentrations is mediated by an enhanced production of PGE2, and that PGE2 operates by stimulating adenylate cyclase (AC) with a consequent rise in cAMP and activation of PKA.

Effects of cholecystokinin, cholecystokinin JMV-180 and GTP analogs on enzyme secretion from permeabilized acini and chloride conductance in isolated zymogen granules of the rat pancreas.

Previous studies have shown that hormonal activation of the Cl- conductance in pancreatic zymogen granules (ZG) is closely related to enzyme secretion from acinar cells. We have now examined the role of guanine nucleotides in stimulated and unstimulated protein secretion from isolated digitonin-permeabilized pancreatic acini and in the Cl- conductance of isolated ZG. Protein secretion from permeabilized isolated acini, measured at 0.1 mM Ca2+, increased with increasing cholecystokinin octapeptide (CCK-8) concentrations and decreased at high CCK-8 concentrations. The maximum secretion, approximately twice the control level, was reached at 1 nM CCK-8. The CCK analog, CCK JMV-180, which supposedly acts as an agonist on high-affinity CCK receptors and as an antagonist on low-affinity CCK receptors, stimulated maximum enzyme secretion at a CCK JMV-180 concentration of 0.1 microM and no decrease in secretion was observed at higher CCK JMV-180 concentrations, 0.1 mM guanosine 5'-[gamma-thio]triphosphate (GTP [S]) also increased the protein release by approximately twice that of the control and shifted the CCK-8 concentration causing maximum stimulation from 1 nM to 0.01 nM. GTP[S] concentrations greater than 0.1 mM inhibited protein release evoked by an optimal concentration of 1 nM CCK-8, 0.1 mM GTP[S] had no pronounced effect on the protein secretion stimulated by low concentrations of CCK JMV-180, but inhibited protein secretion evoked by CCK JMV-180 concentrations greater than 0.1 microM. This indicates that guanosine-nucleotide-binding proteins [G protein(s)] coupling to CCK receptors also mediate both CCK-induced increases and CCK-induced decreases of enzyme secretion at low and high CCK concentrations, respectively. ZG were prepared on a Percoll gradient from CCK-8-stimulated or CCK-JMV-180-stimulated and unstimulated acini. Their Cl- conductances were estimated in the absence of Ca2+ and in the presence of 1 mM EGTA from the rate of decrease in absorbance following addition of the K+ ionophore valinomycin as a measure of ZG osmotic lysis. The Cl- conductance in ZG from CCK-8-stimulated and CCK-JMV-180-stimulated acini was maximally activated at 1 pM and 10 nM respectively. At higher agonist concentrations, Cl- conductance was decreased. Direct addition of 10 microM GTP[S] to isolated ZG from unstimulated acini increased the rate of lysis by approximately 40% of the control value. This effect was approximately additive to that of CCK-8 or of CCK JMV-180 prestimulation.(ABSTRACT TRUNCATED AT 400 WORDS)