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Background: The aim of our study was to analyze perioperative lactate levels and their predictive value for postoperative mortality and morbidity after liver resection. Methods: The clinicopathological characteristics and outcomes of 152 patients who underwent liver resection for benign and malign diagnoses were analyzed retrospectively. Lactate concentrations at three different time points, (1) before liver resection (LAC-PRE), (2) after liver resection on day 0 (LAC-POST), and (3) on day one after the operation (LAC-POD1) were assessed regarding the prognostic value in predicting postoperative complications and mortality according to the Clavien–Dindo (CD) classification. Results: The rates of postoperative complications (CD ≥ IIIb) and mortality rates were 19.7% (N = 30) and 4.6% (N = 7), respectively. The LAC-PRE levels showed no correlation with the postoperative outcome. The ROC curve analysis showed that LCT-POST and LCT-POD1 values were moderately strong in predicting postoperative morbidity (0.681 and 0.768, respectively) and had strong predictive accuracies regarding postoperative mortality (0.800 and 0.838, respectively). The multivariate analysis revealed LAC-POST as a significant predictor of postoperative complications (CD ≥ IIIb: OR 9.28; 95% CI: 2.88–29.9; p < 0.001) and mortality (OR 11.69; 95% CI: 1.76–77.7; p = 0.011). Conclusion: Early postoperative lactate levels are a useful and easily practicable predictor of postoperative morbidity and mortality in patients after liver resection.

Background/AimsAim of our study was to analyze surgical parameters and postoperative morbidity with special emphasis on cut surface biliary leakage (BL), after launching a minimally invasive liver resection program at our center.Patients and methodsA prospectively maintained medical database of patients who required liver resection was used for analysis. Exclusion criteria were liver resections with biliodigestive anastomosis. Clinicopathological characteristics and outcomes were analyzed retrospectively.ResultsA total of 141 patients were divided into a group of 47 patients (33.3%) receiving laparoscopic (LLR) and 94 patients (66.7%) undergoing open liver resections (OLR). We performed 62 major OLR (66.0%) and 31 major LLR (66.0%). In comparison with the LLR group, operation time was longer (326 ± 97 minutes vs. 287 ± 133 minutes; P = 0.080) and average blood loss was higher in the OLR group (529 ± 441 mL vs. 356 ± 459 mL; P = 0.052), without showing significancy. In the LLR group, morbidity was significantly lower than in the OLR group (OLR vs. LLR: 19 (20.2 %) vs. 3 (6.4%); P = 0.033). Overall BL rate was 4.3% (N = 6). All BL occurred in patients after OLR and were associated with a significantly longer hospital stay (hospital stay with biliary leakage vs. hospital stay without biliary leakage: 37.3 ± 19.3 days vs. 14.7 ± 11.1 days; P < 0.001).ConclusionThe introduction of different transection techniques in laparoscopic liver resections did not increase morbidity and BL rate.

Background/AimsBiliary leakage (BL) is a major cause of postoperative morbidity after liver resection. Aim of our study was to analyse surgical parameters and postoperative morbidity with special emphasis on BL, after launching a minimally invasive liver resection program.MethodsA prospectively maintained medical database of patients who required a liver resection was used for analysis.ResultsA total of n=156 patients were divided into a group of n=47 patients (30.1%) receiving laparoscopic (LLR) and n=109 patients (69.9%) undergoing open liver resections (OLR). Patient age (OLR: 59.4 ± 16.0 vs. LLR: 57.9 ± 14.2 years) and male to female ratio (OLR: 63/46 vs. LLR: 25/22) were comparable. We performed n=75 (68.8%) major OLR and n=31 (66.0%) major LLR. Operation time was OLR 342.8 ± 110.5 min vs. LLR 287.3 ± 132.6 min (p=0.014) and the average blood loss was OLR 523.5 ± 428.6 ml vs. LLR 355.5 ± 459.2 ml. Morbidity and mortality was observed in n= 29 (18.6 %) and n= 7 (4.5 %) patients, respectively. The overall biliary leakage (BL) rate was 5.1% (n= 8). Majority of BL were detected in OLR with biliodigestive anastomosis (BDA) (n=2 (11.0%)) followed by OLR without BDA (n=6 (6.5%)). No BL were detected in patients with LLR. Hospital stay was significantly prolonged after OLR in patients with BL (38.4 ± 20.1 vs. 17.4 ± 11.1 days, p< 0.001).ConclusionIn line with previous reports, the introduction of different transection techniques in laparoscopic liver resections did not increase morbidity and BL-rate.

ZusammenfassungDas pädiatrische Emergence Delir rückt aufgrund der Debatte um Neurotoxizität von Anästhetika bei kleinen Kindern erneut in den Fokus. Die 2017 von der Europäischen Gesellschaft für Anästhesiologie (ESA) publizierte Leitlinie zu Prävention und Therapie kann eine sinnvolle Unterstützung der klinischen Tätigkeit sein. Insbesondere die zügige und konsequente Behandlung von Schmerzen bei kleinen Kindern und die konsequente Diagnose eines pädED mittels validierter Skale ermöglicht es- dank der Verbreitung von patient data management systemen- in Zukunft eine reelle Inzidenz des pädEDs anzugeben. In der Prävention des pädED liegt der Schwerpunkt auf der Reduktion der präoperativen Angst der Kinder, egal, ob dies durch ein auf das Kind fokussierte Kinderanästhesieteam zusammen mit den Eltern, Musik, Clowns, smartphones/tablets oder eine medikamentöse Prämedikation erzielt wird. Medikamentöse pädED-Prophylaxe durch perioperative Anwendung von alpha-2-Agonisten und die Verwendung von Propofol als Ausleitungsbolus oder TIVA erscheint gleichzeitg sinnvoll. Postoperativ ermöglicht eine ruhige Aufwachumgebung ein entspanntes delirfreies Aufwachen. Postanästhesiologische Visiten mit strukturiertem Erfassen von Veränderungen des kindlichen Verhaltens respektive schriftliche Fragebögen werden in Zukunft Auskunft über das pädED auf den Normalstationen geben. Strukturierte Nachbefragungen im Verlauf werden auch die Erfassung postoperativen unerwünschten Verhaltensänderungen und deren möglichen Zusammenhang zum pädED ermöglichen.

In March 2019 the HADES experiment recorded 14 billion Ag+Ag collisions at √sNN = 2.55 GeV as a part of the FAIR phase-0 physics program. In this contribution, we present and investigate our capabilities to reconstruct and analyze weakly decaying strange hadrons and hypernuclei emerging from these collisions. The focus is put on measuring the mean lifetimes of these particles.

Notfalle mit Kindern machen ca. 5–10% aller praklinischen Notfalle aus. Invasive Masnahmen zur Sicherung der Atemwege sind davon in weniger als 5% notig [1,2]. Nicht zuletzt aufgrund der insgesamt geringen Inzidenz stellt die Atemwegssicherung bei Kindern daher fur viele praktizierende Notfallmediziner und Rettungskrafte eine grose Herausforderung dar. Es fehlt an der notwendigen Routine im Umgang mit kindlichen Atemwegen bei einer gleichzeitig hohen emotionalen Belastung.

In congenital hyperinsulinism (CHI), the identification and precise localization of a focal lesion is essential for successful surgery.Our objective was to evaluate the predictive value and accuracy of integrated [18F]fluoro-L-DOPA ([18F]FDOPA) positron emission tomography (PET)-computed tomography (CT) for the surgical therapy of CHI.This was an observational study.The study was performed in the Department of Pediatric Surgery at a university hospital.From February 2005 to September 2007, 10 children with the clinical signs of CHI and an increased radiotracer uptake in a circumscribed area of the pancreas in the [18F]FDOPA PET-CT were evaluated.Guided by the [18F]FDOPA PET-CT report, all children underwent partial pancreatic resection, in two cases twice.Correlation of the anatomical findings at surgery with the report of the [18F]FDOPA PET-CT, and the results of surgery and clinical outcome were determined.In nine children the intraoperative situation corresponded exactly to the description of the [18F]FDOPA PET-CT. A limited resection of the pancreas was curative in eight cases at the first surgery, in one case at the second intervention. We observed no diabetes mellitus or exocrine insufficiency in the follow up so far. In one child, hypoglycemia persisted even after two partial resections of the pancreatic head. Histological analysis finally revealed an atypical intermediate form of CHI.The integrated [18F]FDOPA PET-CT is accurate to localize the lesion in focal CHI and is a valuable tool to guide the surgeon in limited pancreatic resection.

Background The objective of this study was to determine whether endothelin-A receptor blockade (ETAB) impairs hemodynamic and hormonal regulation compared with controls and angiotensin II receptor blockade (AT1B) during hypotensive hemorrhage in dogs under isoflurane-nitrous oxide anesthesia. Methods Six dogs were studied in four protocols: (1) control experiments (controls); (2) ETA blockade using ABT-627 (ETAB); (3) AT1 blockade using losartan (AT1B); and (4) combined AT1B and ETAB (AT1B + ETAB). After a 30-min awake period, isoflurane-nitrous oxide anesthesia was established (1.3 minimum anesthetic concentration). After 60 min of anesthesia, 20 ml blood/kg body weight was withdrawn within 5 min, and the dogs were observed for another hour. Thereafter, the blood was retransfused, and the dogs were observed for a final hour. Results Anesthesia: Cardiac output decreased in all protocols, whereas mean arterial pressure decreased more in AT1B and AT1B + ETAB than in controls and ETAB. Hemorrhage: After 60 min, cardiac output had decreased less in controls than in all other protocols. Mean arterial pressure decreased more during ETAB than in controls, but most severely during AT1B and AT1B + ETAB. Angiotensin II increased further only in controls and ETAB, whereas vasopressin and catecholamines increased similarly in all protocols. Retransfusion: Mean arterial pressure remained below controls in all protocols but was lowest when the AT1 receptor was blocked. Cardiac output fully recovered in all but the ETAB protocol. Conclusions ETAB impairs long-term hemodynamic regulation after hemorrhage and retransfusion during anesthesia despite an activation of vasoconstrictive hormones. This suggests that endothelins have a role in long-term cardiovascular regulation. AT1B impairs both short- and long-term blood pressure regulation during anesthesia and after hemorrhage.

Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of hypoxia-induced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-sodium (LS = 0.5 mmol sodium · kg body wt−1· day−1) or high-sodium (HS = 7.5 mmol sodium · kg body wt−1· day−1) diet. The dogs breathed spontaneously via a ventilator circuit during the experiments: first hour, normoxia (inspiratory oxygen fraction = 0.21); second to fourth hour, hypoxia (inspiratory oxygen fraction = 0.1). During hypoxia (arterial Po234.4 ± 2.1 Torr), plasma pH increased from 7.37 ± 0.01 to 7.48 ± 0.01 ( P < 0.05) because of hyperventilation (arterial Pco225.6 ± 2.4 Torr). Urinary pH and urinary bicarbonate excretion increased irrespective of the sodium intake. Sodium excretion increased more during HS than during LS, whereas the increase in potassium excretion was comparable in both groups. Thus the quick onset of bicarbonate excretion within the first hour of hypoxia-induced respiratory alkalosis was not impaired by a low sodium intake. The increased sodium excretion during hypoxia seems to be combined with a decrease in plasma aldosterone and angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.

This study investigated whether adenosine mediates the decrease in plasma renin activity (PRA) during acute hypoxia. Eight chronically tracheotomized, conscious beagle dogs were kept under standardized environmental conditions and received a low-sodium diet (0.5 mmol · kg body wt−1 · day−1). During the experiments, the dogs were breathing spontaneously via a ventilator circuit: first hour, normoxia (21% inspiratory concentration of O2); second and third hours, hypoxia (10% inspiratory concentration of O2). Each of the eight dogs was studied twice in randomized order in control and theophylline experiments. In theophylline experiments, theophylline, an A1-receptor antagonist, was infused intravenously during hypoxia (loading dose: 3 mg/kg within 30 min, maintenance: 0.5 mg · kg−1 · h−1). In theophylline experiments, PRA (5.9 ± 0.8 ng ANG I · ml−1 · h−1) and ANG II plasma concentration (15.9 ± 2.3 pg/ml) did not decrease during hypoxia, whereas plasma aldosterone concentration decreased from 277 ± 63 to 132 ± 23 pg/ml ( P < 0.05). In control experiments, PRA decreased from 6.8 ± 0.8 during normoxia to 3.0 ± 0.5 ng ANG I · ml−1 · h−1 during hypoxia, ANG II decreased from 13.3 ± 1.9 to 7.3 ± 1.9 pg/ml, and plasma aldosterone concentration decreased from 316 ± 50 to 70 ± 13 pg/ml ( P < 0.05). Thus infusion of the adenosine receptor antagonist theophylline inhibited the suppression of the renin-angiotensin system during acute hypoxia. The decrease in aldosterone occurred independently and is apparently directly related to hypoxia. In conclusion, it is likely that adenosine mediates the decrease in PRA during acute hypoxia in conscious dogs.

Part 0: General Introduction.- Part I: Bulk Properties of Strongly Interacting Matter.- Part II: In-Medium Excitations.- Part III Collision Dynamics.- Part IV: Observables and Predictions.- Part V The CBM Experiment.- Glossary.- References.

The noble gas xenon seems to have minimal cardiovascular side-effects and so may be an ideal anaesthetic agent when investigating cardiovascular physiology. In comparison with standard modern anaesthetics, we investigated the haemodynamic and hormonal effects of xenon in Beagle dogs. After a 30 min baseline period, anaesthesia was induced with propofol and maintained with either (1) 1.2% isoflurane/70% nitrous oxide (N2O), (2) 0.8% isoflurane/0.5 µg/kg/min remifentanil or (3) 63% xenon/0.5 µg/kg/min remifentanil ( n = 6 per group). Haemodynamics were recorded and blood samples taken before and 60 min after induction. Mean arterial blood pressure (MAP) was higher in conscious dogs than during isoflurane/N2O (86 ± 2 vs. 65 ± 2 mmHg, mean ± SEM) and isoflurane/remifentanil anaesthesia (95 ± 2 vs. 67 ± 3 mmHg), whereas MAP did not decrease significantly in response to xenon/remifentanil anaesthesia (96 ± 4 vs. 85 ± 6 mmHg). Bradycardia was present during isoflurane/remifentanil (54 ± 2/min) and xenon/remifentanil (40 ± 3/min), but not during isoflurane/N2O anaesthesia (98 ± 3/min, P < 0.05). Xenon/remifentanil anaesthesia induced the highest reduction in cardiac output (CO) (–61%), and the highest increase in systemic vascular resistance (+120%) among all treatment groups ( P < 0.05). A simultaneous increase in endogenous adrenaline and noradrenaline concentrations could only be observed in the xenon/remifentanil group, whereas angiotensin II and vasopressin concentrations increased in all groups. In conclusion, xenon/remifentanil anaesthesia maintains MAP but reduces heart rate and CO and is associated with a considerable stimulation of vasopressor hormones in Beagle dogs. Therefore, xenon/remifentanil exerts a new quality of adverse haemodynamic effects different from volatile anaesthetics and may not perform better during studies of cardiovascular physiology.

Acute hypoxic pulmonary vasoconstriction can be inhibited by high doses of the carbonic anhydrase inhibitor acetazolamide. This study aimed to determine whether acetazolamide is effective at dosing relevant to human use at high altitude and to investigate whether its efficacy against hypoxic pulmonary vasoconstriction is dependent on carbonic anhydrase inhibition by testing other potent heterocyclic sulfonamide carbonic anhydrase inhibitors. Six conscious dogs were studied in five protocols: 1) controls, 2) low-dose intravenous acetazolamide (2 mg·kg−1·h−1), 3) oral acetazolamide (5 mg/kg), 4) benzolamide, a membrane-impermeant inhibitor, and 5) ethoxzolamide, a membrane-permeant inhibitor. In all protocols, unanesthetized dogs breathed spontaneously during the first hour (normoxia) and then breathed 9–10% O2 for the next 2 h. Arterial oxygen tension ranged between 35 and 39 mmHg during hypoxia in all protocols. In controls, mean pulmonary artery pressure increased by 8 mmHg and pulmonary vascular resistance by 200 dyn·s·cm−5 ( P −5 during hypoxia ( P < 0.05). Low-dose acetazolamide is effective against acute hypoxic pulmonary vasoconstriction in vivo. The lack of effect with two other potent carbonic anhydrase inhibitors suggests that carbonic anhydrase is not involved in the mediation of hypoxic pulmonary vasoconstriction and that acetazolamide acts on a different receptor or channel.

Acute hypoxia increases pulmonary arterial pressure and vascular resistance. Previous studies in isolated smooth muscle and perfused lungs have shown that carbonic anhydrase (CA) inhibition reduces the speed and magnitude of hypoxic pulmonary vasoconstriction (HPV). We studied whether CA inhibition by acetazolamide (Acz) is able to prevent HPV in the unanesthetized animal. Ten chronically tracheotomized, conscious dogs were investigated in three protocols. In all protocols, the dogs breathed 21% O2for the first hour and then 8 or 10% O2for the next 4 h spontaneously via a ventilator circuit. The protocols were as follows: protocol 1: controls given no Acz, inspired O2fraction (FiO2) = 0.10; protocol 2: Acz infused intravenously (250-mg bolus, followed by 167 μg·kg−1·min−1continuously), FiO2= 0.10; protocol 3: Acz given as above, but with FiO2reduced to 0.08 to match the arterial Po2(PaO2) observed during hypoxia in controls. PaO2was 37 Torr during hypoxia in controls, mean pulmonary arterial pressure increased from 17 ± 1 to 23 ± 1 mmHg, and pulmonary vascular resistance increased from 464 ± 26 to 679 ± 40 dyn·s−1·cm−5( P < 0.05). In both Acz groups, mean pulmonary arterial pressure was 15 ± 1 mmHg, and pulmonary vascular resistance ranged between 420 and 440 dyn·s−1·cm−5. These values did not change during hypoxia. In dogs given Acz at 10% O2, the arterial PaO2was 50 Torr owing to hyperventilation, whereas in those breathing 8% O2the PaO2was 37 Torr, equivalent to controls. In conclusion, Acz prevents HPV in conscious spontaneously breathing dogs. The effect is not due to Acz-induced hyperventilation and higher alveolar Po2, nor to changes in plasma endothelin-1, angiotensin-II, or potassium, and HPV suppression occurs despite the systemic acidosis with CA inhibition.

The objective of this study was to determine whether endothelin-A receptor blockade (ETAB) impairs hemodynamic and hormonal regulation compared with controls and angiotensin II receptor blockade (AT1B) during hypotensive hemorrhage in dogs under isoflurane-nitrous oxide anesthesia.Six dogs were studied in four protocols: (1) control experiments (controls); (2) ETA blockade using ABT-627 (ETAB); (3) AT1 blockade using losartan (AT1B); and (4) combined AT1B and ETAB (AT1B + ETAB). After a 30-min awake period, isoflurane-nitrous oxide anesthesia was established (1.3 minimum anesthetic concentration). After 60 min of anesthesia, 20 ml blood/kg body weight was withdrawn within 5 min, and the dogs were observed for another hour. Thereafter, the blood was retransfused, and the dogs were observed for a final hour.Anesthesia: Cardiac output decreased in all protocols, whereas mean arterial pressure decreased more in AT1B and AT1B + ETAB than in controls and ETAB. Hemorrhage: After 60 min, cardiac output had decreased less in controls than in all other protocols. Mean arterial pressure decreased more during ETAB than in controls, but most severely during AT1B and AT1B + ETAB. Angiotensin II increased further only in controls and ETAB, whereas vasopressin and catecholamines increased similarly in all protocols. Retransfusion: Mean arterial pressure remained below controls in all protocols but was lowest when the AT1 receptor was blocked. Cardiac output fully recovered in all but the ETAB protocol.ETAB impairs long-term hemodynamic regulation after hemorrhage and retransfusion during anesthesia despite an activation of vasoconstrictive hormones. This suggests that endothelins have a role in long-term cardiovascular regulation. AT1B impairs both short- and long-term blood pressure regulation during anesthesia and after hemorrhage.

The Compressed Baryonic Matter (CBM) experiment at the future FAIR accelerator complex at Darmstadt is being designed for a comprehensive measurement of hadron and lepton production in heavy-ion collisions from 8-45 AGeV beam energy, producing events with large track multiplicity and high hit density. The setup consists of several detectors including as tracking detectors the silicon tracking system (STS), the muon detector (MUCH) or alternatively a set of Transition Radiation Detectors (TRD). In this contribution, the status of the track reconstruction software including track finding, fitting and propagation is presented for the MUCH and TRD detectors. The track propagation algorithm takes into account an inhomogeneous magnetic field and includes accurate calculation of multiple scattering and energy losses in the detector material. Track parameters and covariance matrices are estimated using the Kalman filter method and a Kalman filter modification by assigning weights to hits and using simulated annealing. Three different track finder algorithms based on track following have been developed which either allow for track branches, just select nearest hits or use the mentioned weighting method. The track reconstruction efficiency for central Au+Au collisions at 25 AGeV beam energy using events from the UrQMD model is at the level of 93-95% for both detectors.