Second-generation argon plasma coagulation: two-center experience with 600 patients.

BACKGROUND AND AIM: Second-generation argon plasma coagulation (APC; APC 2/VIO APC) with its modes 'forced', 'pulsed', and 'precise' is a further development of the ICC/APC 300 system (first-generation APC). Until now, only limited data has existed on the use of APC 2. METHODS: Fundamental data on the characteristics of the various APC 2 modes and clinical data from more than 600 patients treated in two high-volume endoscopy centers were analyzed. On the basis of these data, recommendations for the use of APC in daily gastroenterological practice were made. RESULTS: In comparison to the ICC system, second-generation APC offers a broadened bandwidth of settings including different APC modes and a range of power settings from 1 to 120 W. Using the various modes of APC 2 in a variety of gastrointestinal diseases, minor complications were observed in 9-21% of patients. Major complications occurred in 1-7% of patients. CONCLUSIONS: In a two-center experience treating a large group of patients with a wide variety of gastrointestinal conditions, the different APC 2 modes appeared to be safe and effective. Certain preventive measures before and during clinical application are recommended in order to avoid complications.

Successful treatment of catastrophic antiphospholipid antibody syndrome (CAPS) associated with splenic marginal-zone lymphoma with low-molecular weight heparin, rituximab and bendamustine.

CASE REPORT: A 69-year-old woman with splenic marginal-zone lymphoma was admitted with progressive abdominal pain and splenomegaly as the suspected cause of pain. Rituximab treatment (375 mg/m) had been initiated on the day of admission. Abdominal computerized tomography revealed splenic infarction. Laboratory tests showed elevation of liver enzymes and creatinine, low platelet count, prolonged partial thromboplastin time, and lupus anticoagulant positivity. The diagnosis of catastrophic antiphospholipid antibody syndrome was made. Weight-adjusted low-molecular weight heparin therapy was initiated. Freedom from symptoms and normalization of liver enzymes and creatinine occurred within 4 weeks. Treatment was continued with 6 cycles of bendamustine monotherapy (90 mg/m) and heparin, leading to partial remission of lymphoma and lupus anticoagulant negativity. CONCLUSIONS: In case of multiorgan failure in patients suffering from lymphoma and showing features of disseminated intravascular coagulation, catastrophic antiphospholipid antibody syndrome should be considered. In our patient, rituximab followed by weight-adjusted low-molecular weight heparin and bendamustine therapy led to recovery.

C1-esterase inhibitor reverses functional consequences of superior mesenteric artery ischemia/reperfusion by limiting reperfusion injury and restoring microcirculatory perfusion.

Activated complement contributes significantly to reperfusion injury after ischemia. This study explores functional consequences of C1-esterase inhibitor (C1-INH) treatment after superior mesenteric artery occlusion (SMAO)/reperfusion using intravital microscopy. Thirty anesthetized, spontaneously breathing, male Sprague-Dawley rats underwent SMAO for 60 min followed by reperfusion (4 h). C1-esterase inhibitor (100 and 200 IU/kg body weight) or saline (0.9%) was given as a single bolus before reperfusion. Sham-operated animals (n = 10) without SMAO served as controls. Systemic hemodynamics were monitored continuously, arterial blood gases analyzed intermittently, and leukocyte/endothelial interactions in the mesenteric microcirculation quantified at intervals using intravital microscopy. Ileal lipid-binding protein (I-LBP) levels were determined from serum samples with an enzyme-linked immunosorbent assay at the end of the experiments. C1-esterase inhibitor restored microcirculatory perfusion to baseline levels in a dose-dependent manner and reduced adherent leukocytes after SMAO/reperfusion to similar levels in both C1-INH-treated groups during reperfusion. Furthermore, C1-INH treatment efficiently prevented metabolic acidosis, reduced the need for intravenous fluids to support blood pressure, and decreased I-LBP levels in a dose-dependent manner. Survival rates were 100% in controls and after 200 IU/kg C1-INH, 90% after 100 IU/kg C1-INH, and 30% in saline-treated animals. C1-esterase inhibitor bolus infusion efficiently blunted functional consequences of mesenteric ischemia/reperfusion with I-LBP, proving to be a valuable serum marker mirroring the effect of ischemia/reperfusion and treatment at the end of the experiments.

Prolonged recirculation is required to detect secondary metabolic and hemodynamic deterioration after superior mesenteric artery occlusion.

We evaluated late (4 hrs) effects of reperfusion on hemodynamics after 30 or 60 min occlusion of the superior mesenteric artery (SMA) in a rat model. Spontaneously breathing animals (n=30) underwent occlusion of the SMA for 0 (sham), 30 (SMAO_30) or 60 min (SMAO_60) followed by reperfusion with normal saline. Abdominal blood flow (ABF), SMA blood flow (SBF), arterial blood pressure and heart rate were recorded continuously. Systemic vascular resistance (SVR) and SMA vascular resistance (MVR) were calculated at baseline and after 240 min reperfusion (240R). All animals survived in SMAO_30 and sham, two died in SMAO_60 after 120R. ABF remained constant in all groups. SVR increased in SMAO_30 and sham and decreased in SMAO_60 at 240R. SBF was significantly lower after reperfusion in ischemia groups as compared to sham. After 120R, SBF had increased significantly in SMAO_60 versus SMAO_30. MVR increased significantly in SMAO_30 but not in SMAO_60 and sham at 240R. 60 minutes SMA occlusion revealed early hemodynamic changes of septic circulation with increased blood flow in the SMA, decreased SVR, and pseudo-normalization of MVR. Prolonged observation periods are required to detect these significant changes which are overlooked when only studying 120 minutes of reperfusion as usually done.

The tissue effect of second generation argon plasma coagulation (VIO APC) in comparison to standard APC and Nd:YAG laser in vitro.

BACKGROUND: The aim of this study was to evaluate the effect of 2nd generation argon plasma coagulation (VIO APC) with respect to the tissue destruction capacity, and to compare it with standard APC and Nd:YAG laser. METHODS: 2nd generation APC (VIO APC2, Erbe, Germany), standard APC (APC 300/Erbotom ICC 200, Erbe) and Nd:YAG laser (KTP/YAG XP 800; Laserscope, San Jose, California) were applied in 35 porcine livers. Using APC, power settings (30-120 W), application time (2 and 5 sec) and gas flow (1 and 2 l/min) were varied. Using Nd:YAG laser, 30-60 W were applied (flow 21/min). Diameter and depth of tissue coagulation were evaluated. RESULTS: Using VIO APC, maximum coagulation depth was 6 mm (maximum diameter 15 mm). In comparison to standard APC, the coagulation effect was significantly higher (p < 0.001). There was no significant difference in the mean depth achieved by VIO APC and Nd:YAG laser using 30- 60 W and an application time of 2 sec (p < 0.05). Using maximum energy available for the 2 systems, maximum depth achieved by VIO APC (6 mm) was higher than the one caused by Nd:YAG laser (4 mm). CONCLUSIONS: VIO APC was more effective than standard APC. Using medium power and a limited application time, it was as effective as Nd:YAG laser. The high effectiveness of VIO APC should be a topic of clinical education.

Shunting of the microcirculation after mesenteric ischemia and reperfusion is a function of ischemia time and increases mortality.

OBJECTIVE: Shunting of the microcirculation contributes to the pathology of sepsis and septic shock. The authors address the hypothesis that shunting of the microcirculation occurs after superior mesenteric artery occlusion (SMAO) and reperfusion, and explore functional consequences. METHODS: Spontaneously breathing animals (rats) (n = 30) underwent SMAO for 0 (controls), 30 (SMAO_30) or 60 min (SMAO_60) followed by reperfusion (4 h) with normal saline. Leukocyte-endothelial interactions in mesenteric venules were quantified in an exteriorized ileal loop using intravital microscopy. Abdominal blood flow was recorded continuously, and arterial blood gases were analyzed at intervals. The above groups were matched by comparable groups with continuous superior mesenteric artery blood flow measurements and without exteriorizing an ileal loop (controls*, SMAO_30*, SMAO_60*). RESULTS: Adherent leukocytes increased shortly after reperfusion in ischemia groups, and plateaued in these groups. Centerline velocity in the recorded venules was significantly reduced after reperfusion down to low-flow/no-flow in SMAO_60 as compared to SMAO_30 and controls, whereas perfusion of the SMA and ileal vessels persisted. The microcirculatory changes in SMAO_60 were accompanied by progressive metabolic acidosis, substantially larger volumes of intravenous fluids needed to support arterial blood pressure and significantly reduced survival (30%). SMA blood flow increased in relation to abdominal blood flow after reperfusion in SMAO_60*, and remained constant in SMAO_30* and controls*. Survival was 80% in SMAO_60*. CONCLUSION: Shunting of the microcirculation can be observed after SMAO for 60 min and reperfusion, and contributes significantly to the pathology of mesenteric ischemia and poor outcome.