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To compare surgical versus medical treatment of type 2 diabetes mellitus (T2DM) remission and comorbidities in patients with a body mass index (BMI) less than 35 kg/m2.Obesity surgery can achieve remission of T2DM and its comorbidities. Metabolic surgery has been proposed as a treatment option for diabetic patients with BMI less than 35 kg/m2 but the efficacy of metabolic surgery has not been conclusively determined.A systematic literature search identified randomized (RCT) and nonrandomized comparative observational clinical studies (OCS) evaluating surgical versus medical T2DM treatment in patients with BMI less than 35 kg/m2. The primary outcome was T2DM remission. Additional analyses comprised glycemic control, BMI, HbA1c level, remission of comorbidities, and safety. Random effects meta-analyses were calculated and presented as weighted odds ratio (OR) or mean difference (MD) with 95% confidence intervals (95% CI).Five RCTs and 6 OCSs (706 total T2DM patients) were included. Follow-up ranged from 12 to 36 months. Metabolic surgery was associated with a higher T2DM remission rate (OR: 14.1, 95% CI: 6.7-29.9, P0.001), higher rate of glycemic control (OR: 8.0, 95% CI: 4.2-15.2, P0.001) and lower HbA1c level (MD: -1.4%, 95% CI -1.9% to -0.9%, P0.001) than medical treatment.-5.5 kg/m2, 95% CI: -6.7 to -4.3 kg/m2, P0.001), rate of arterial hypertension (OR: 0.25, 95% CI: 0.12-0.50, P0.001) and dyslipidemia (OR: 0.21, 95% CI: 0.10-0.44, P0.001) were lower after surgery.Metabolic surgery is superior to medical treatment for short-term remission of T2DM and comorbidities. Further RCTs should address the long-term effects on T2DM complications and mortality.

Comparison of two different insertion techniques for implantation of totally implantable access ports (TIAP).TIAP are introduced through different open and closed cannulation strategies and by various medical experts. The aim of this expertise-based randomized trial was to compare venous cutdown approach with puncture of subclavian vein.One hundred and ten patients scheduled for primary implantation of a TIAP were randomly assigned to either open insertion technique performed by surgeons or puncture of the subclavian vein under fluoroscopic guidance by radiologists at an outpatient single university center. The primary endpoint was the primary success rate of the cannulation strategy. A logistic regression model was used for analysis adjusting for age, Karnofsky index, body mass index and surgeons', and the radiologists' experience.Percutaneus cannulation was not superior to surgical venous cutdown in the intention-to-treat analysis (odds ratio, 0.37; 95% CI, 0.07; 2.15) and the as-treated analysis (odds ratio, 0.16; 95% CI, 0; 1.28). The procedure was shorter with surgery (median, 21 minutes; 95% CI, 14; 30) than with radiology (median, 45 minutes; 95% CI, 43; 50) (P0.001), and the dose of radiation was lower with surgery (median, 37 cGy/cm(2); 95% CI, 26; 49) than with radiology (200 cGy/cm(2); 95% CI, 200; 300) (P0.001).Central venous cannulation for insertion of TIAPs can be performed safely and effectively with both approaches. The open direct surgical access requires further strategies for successful placement of a TIAP, and percutaneous Seldinger technique requires more time and a higher dose of radiation and is associated with risk of pneumothorax.

Background Thoracic epidural anesthesia (TEA) protects the intestinal microcirculation and improves perioperative outcomes. TEA also reduces mortality in acute experimental pancreatitis. Its impact on hepatic microcirculation, however, in health and critical illness is unknown. Therefore, the authors studied the effect of TEA on the liver in healthy rats and in experimental severe acute pancreatitis. Methods TEA was induced by 15 microl/h bupivacaine, 0.5%. Necrotizing pancreatitis was induced by intraductal infusion of 2 ml/kg taurocholic acid, 5%. Twenty-eight rats were assigned to either Sham operation, Sham + TEA, Pancreatitis, or Pancreatitis + TEA. After 15 h, mean arterial pressure, heart rate, and respiratory function were recorded. Sinusoidal width and perfusion rate and the intrahepatic leukocyte adhesion were assessed by intravital microscopy. In an additional 22 rats randomly assigned to Sham, Pancreatitis, and Pancreatitis + TEA, hepatic apoptosis was evaluated by staining for single-stranded DNA and Fas ligand-positive cells. Results TEA did not affect hepatic microcirculation and leukocyte adhesion in healthy rats. Blood pressure remained unchanged in the Sham + TEA group. In Pancreatitis, mean arterial pressure decreased from 141 + or - 6 mmHg to 127 + or - 13 mmHg but remained stable in Pancreatitis + TEA. The sinusoidal diameter decreased from 5.4 + or - 0.1 microm to 5.0 + or - 0.2 microm in Pancreatitis. This was restored in Pancreatitis + TEA. Intrahepatic leukocyte adhesion was not affected by TEA. The increased hepatocyte apoptosis in Pancreatitis was abolished in Pancreatitis + TEA. This might be mediated by inhibition of the Fas ligand pathway. Conclusion TEA reduces liver injury in necrotizing acute pancreatitis. This could be related to a regional sympathetic block. TEA could thus preserve liver function in systemic inflammatory disorders such as acute pancreatitis.

Thoracic epidural anesthesia (TEA) is most frequently used after major surgery. However, despite ongoing research, the influence of TEA on the intestinal perioperative pathophysiology is not fully understood.According to recent results, the splanchnic sympathetic activity is reduced during TEA both in animal models and in clinical TEA. The splanchnic sympathetic activity during high TEA is still unknown. Intestinal perfusion effects of TEA are still unclear as the technique and extent of TEA, hemodynamic alteration and size of measurement result in--seemingly--conflicting reports. Postoperative ileus after laparotomy is ameliorated by TEA. Recent findings suggest beneficial effects also after major laparoscopic procedures. Finally, the impact of TEA on the intestinal pathophysiology in critical illness is an area of growing clinical and scientific interest, although this knowledge is just at its beginning.Further research concerning the use of TEA in major laparoscopic procedures and its potential to improve or endanger anastomotic healing is warranted. The experimental studies of TEA in critical illness should be expanded.

Background Clinical benefits of thoracic epidural anesthesia (TEA) are partly ascribed to thoracic sympathetic block. However, data regarding sympathetic activity during TEA are scarce and contradictory. This prospective, randomized, double-blind study evaluated the segmental propagation of sympathetic block after low-concentration, high-volume TEA using digital thermography. Methods Twenty-four patients were included in the study. Thoracic epidural catheters were placed at a median insertion level of T8-T9. Patients were accommodated for 20 min to the room temperature of 23 degrees +/- 0.3 degrees C. Skin temperature was recorded by digital thermography. After baseline measurement of heart rate, arterial pressure, and core body and skin temperature, 10 ml saline (control group) or 10 ml bupivacaine, 0.25% (TEA group), respectively, was administered epidurally. Five minutes (t5) and 20 min (t20) after baseline measurements, hemodynamic parameters and core body temperature were again measured, and sensory block was identified by loss of cold-warm discrimination. In the thumb, the toe, and each thoracic dermatome, difference from baseline temperature was calculated at t5 and t20. Data were analyzed by Mann-Whitney U test. Results Baseline characteristics did not differ among groups. Median spread of sensory block at t20 was T5-L5. At both t5 and t20, skin temperature decreased more in the control group than in the TEA group in all thoracic dermatomes (P < 0.05). Toe temperature increased in the TEA group compared with the control group (P < 0.05), whereas thumb temperature remained unchanged. Conclusion TEA with 10 ml bupivacaine, 0.25%, induced thoracic and lumbar sympathetic block that precedes and exceeds sensory block. Caudal limit of sympathetic block could not be demonstrated in this study.

Background Acute pancreatitis has been linked to intestinal barrier dysfunction and systemic inflammatory response with high mortality. Thoracic epidural analgesia improves intestinal perfusion. The authors hypothesized that thoracic epidural analgesia influences microcirculation injury, inflammatory response, and outcome of acute pancreatitis in rats. Methods Control groups underwent a sham procedure or untreated pancreatitis induced by intraductal taurocholate injection. In the treatment groups, epidural analgesia was commenced immediately or after a 7-h delay. Fifteen hours after injury, the ileal mucosal perfusion was assessed by intravital microscopy. Thereby, the intercapillary area between all perfused capillaries and between continuously perfused capillaries only was used to differentially quantify total and continuous capillary mucosal perfusion. Villus blood flow and serum levels of amylase, lactate, and interleukin 6 were determined, and pancreatic injury was scored histologically. Seven-day survival was recorded in an additional 30 rats undergoing untreated pancreatitis or pancreatitis with epidural analgesia. Results In untreated pancreatitis, decreased total capillary perfusion increased the total intercapillary area by 24%. Furthermore, loss of continuous perfusion increased continuous intercapillary area to 228%. After immediate and delayed epidural analgesia, continuous perfusion was restored (P < 0.05). Blood flow decreased 50% in untreated pancreatitis but was preserved by epidural analgesia (P < 0.05). Biochemical and histologic signs of pancreatitis were not affected by epidural analgesia. Lactate and interleukin-6 levels increased in untreated pancreatitis, which was prevented in the treatment groups (P < 0.05). Epidural analgesia increased 7-day survival from 33% to 73% (P < 0.05). Conclusion Thoracic epidural analgesia attenuated systemic response and improved survival in severe acute pancreatitis. These effects might be explained by improved mucosal perfusion.

Purpose Traditionally, liver surgery relies on Couinaud's liver segment classification. As the position and shape of these segments are variable and their borders are hidden within the homogeneous liver mass, the accuracy of segment identification methods needs computer-aided reevaluation. Method The segmental liver anatomy of 23 patients receiving diagnostic helical CT scans because of suspected intrahepatic lesion was analyzed with the aid of a computer-based operation-planning system. We compared the standard Couinaud classification, which depends particularly on the main stems of portal and hepatic veins, with a method that calculates the segment borders by analyzing the complete portal venous tree. Volume, shape, and position of the liver segments found by each method were compared. Results With reference to the portal vein-based method, segmental volumes were overestimated by the classic Couinaud method by up to 24% and underestimated to 13%. Volumes of Couinaud segments 4a, 7, and 8 were generally larger compared with those obtained by the portal vein-based method, whereas segments 3 and 6 were smaller. Gross variations were found in segments 5, 7, and 8. When shape and position were considered, poor correlation was found for five segments (median kappa = 0.35-0.45). Only segments 2, 7, and 8 had kappa values clearly above 0.45 in the majority of cases. The plane that divides the two hemilivers along the middle hepatic vein and the border between the left sector (segments 2 and 3) and the medial sector (4a and 4b) were found in both methods with very good conformity (kappa > 0.75). Conclusion Couinaud's method of dividing the liver into eight autonomous liver segments has to be accepted as a good approximation. Nevertheless, the volume, position, and shape of these segments and their segmental borders show significant variability.

UNLABELLED Nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) mediates hypotension and metabolic derangements in sepsis. We hypothesized that selective iNOS-inhibition would prevent hypotension in septic rats without inhibiting endothelium-dependent vasodilation caused by the physiologically important endothelial NOS. Rats were exposed to lipopolysaccharide (LPS) for 6 h and the selective iNOS-inhibitor L-N6-(1-iminoethyl)-lysine (L-NIL), the nonselective NOS-inhibitor N:(G)-nitro-L-arginine methyl ester (L-NAME), or control. Mean arterial pressure (MAP) and vasodilation to acetylcholine (ACh, endothelium-dependent), sodium nitroprusside (SNP, endothelium-independent), and isoproterenol (ISO, endothelium-independent beta agonist) were determined. Exhaled NO, nitrate/nitrite-(NOx) levels, metabolic data, and immunohistochemical staining for nitrotyrosine, a tracer of peroxynitrite-formation were also determined. In control rats, L-NAME increased MAP, decreased the response to ACh, and increased the response to SNP, whereas L-NIL did not alter these variables. LPS decreased MAP by 18% +/- 1%, decreased vasodilation (ACh, SNP, and ISO), increased exhaled NO, NOx, nitrotyrosine staining, and caused acidosis and hypoglycemia. L-NIL restored MAP and vasodilation (ACh, SNP, and ISO) to baseline and prevented the changes in exhaled NO, NOx, pH, and glucose levels. In contrast, L-NAME restored MAP and SNP vasodilation, but did not alter the decreased response to ACh and ISO or prevent the changes in exhaled NO and glucose levels. Finally, L-NIL but not L-NAME decreased nitrotyrosine staining in LPS rats. In conclusion, L-NIL prevents hypotension and metabolic derangements in septic rats without affecting endothelium-dependent vasodilation whereas L-NAME does not. IMPLICATIONS Sepsis causes hypotension and metabolic derangements partly because of increased nitric oxide. Selective inhibition of nitric oxide produced by the inducible nitric oxide synthase enzyme prevents hypotension and attenuates metabolic derangements while preserving the important vascular function associated with endothelium-dependent vasodilation in septic rats.