Mario Hensel

Hyperprocalcitonemia in patients with noninfectious SIRS and pulmonary dysfunction associated with cardiopulmonary bypass

Background The incidence of noninfectious systemic inflammatory response syndrome (SIRS) associated with coronary artery bypass surgery and the potential role of several inflammatory parameters as early markers of pulmonary dysfunction induced by cardiopulmonary bypass (CPB) were investigated. Methods Forty patients undergoing elective coronary artery bypass surgery were studied prospectively. Perioperative lung function was monitored using the lung injury score introduced by Murray and colleagues, by measuring venous admixture (Qs/Qt), and, in some cases, by measuring extravascular lung water. Serum concentrations of the inflammatory parameters (procalcitonin, interleukin‐6, sL‐selectin, leukocyte elastase, neopterin, leukocyte counts, and C‐reactive protein) were determined sequentially. The American College of Chest Physicians‐Society of Critical Care Medicine classification system was used to diagnose SIRS. Results According to the entry criteria, SIRS developed in 17 (42%) patients after operation. Nine patients of this group showed signs of acute pulmonary impairment, whereas patients without SIRS had no lung injury. In all patients with acute lung injury, distinct increases in procalcitonin concentrations ranging from 5.1 to 14.3 ng/ml were measured. In patients with SIRS but without acute lung injury and in patients without SIRS, none or only negligible increases in serum concentrations of procalcitonin were seen. Compared with procalcitonin, other inflammatory parameters investigated were less sensitive and less specific to indicate pulmonary dysfunction secondary to CPB. Conclusions Procalcitonin seems to be an appropriate parameter indicating the early development of severe noninfectious SIRS and for predicting pulmonary dysfunction secondary to CPB.

Transient Ca2+ changes in endothelial cells induced by low doses of reactive oxygen species: Role of hydrogen peroxide

Cultured human and rat endothelial cells were used to study cellular toxicity and Ca2+ signalling upon exposure to reactive oxygen species. Superoxide and hydrogen peroxide (O2·–/H2O2) were produced by the hypoxanthine/xanthine oxidase system (HX/XO) and caused intracellular Ca2+ concentration ([Ca2+]i) to rise steadily when activities above 2 mU/ml were used. These Ca2+ increases were also measured when the glucose/glucose oxidase (G/GO) system above 5 mU/ml was used to produce hydrogen peroxide (H2O2). Gross morphological changes appeared to parallel elevated [Ca2+]i levels preceding cell death. However, when HX/XO or G/GO were used at non toxic doses rapid and transient changes in [Ca2+]i were measured. These treatments did not alter subsequent receptor mediated Ca2+ signalling induced by ATP (10 μM) or histamine (100 μM). Superoxide dismutase (50 U/ml), which dismutates O2·minus; into H2O2 al ient [Ca2+]i responses. H2O2 added directly was able to induce similar Ca2+ transients when concentrations of at least 500 μM were used. Buffering trace amounts of iron (o-phenanthroline; 200 μM) in order to inhibit úOH radical formation was not effective to alter Ca2+ changes. Experiments performed in Ca2+-free buffer showed a similar rise in [Ca2+]i and readdition of Ca2+ to the extracellular medium indicated the activation of store operated Ca2+ entry. Blocking Ca2+-ATPases of the endoplasmatic reticulum with thapsigargin (1 μM) inhibited ROS induced transient increases and cells preincubated with pertussis toxin (200 nM) showed unchanged Ca2+ transients after exposure to both enzyme systems. Phospholipase C inhibitor U73122 (2 μM) effectively reduced hydrogen peroxide induced emptying of intracellular stores. Taken together, we demonstrate that enzymatically produced non-toxic H2O2 rather than O· ndash; or · OH causes calcium signalling from thapsigargin sensitive stores, and activates store operated Ca2+ entry at least partially by activating phospholipase C. These changes clearly differ from pathological ‘oxidative stress’ associated with a progressive increase in [Ca2+]i.

A Comparison of Seal in Seven Supraglottic Airway Devices Using a Cadaver Model of Elevated Esophageal Pressure

BACKGROUND:Supraglottic airway devices are increasingly important in clinical anesthesia and prehospital emergency medicine, but there are only few data to assess the risk for aspiration. We designed this study to compare the seal of seven supraglottic airway devices in a cadaver model of elevated esophageal pressure. METHODS:The classic laryngeal mask airway, laryngeal mask airway ProSeal™, intubating laryngeal mask airway Fastrach™, laryngeal tube™, laryngeal tube LTS II™, Combitube™, and Easytube™ were inserted into unfixed human cadavers with an exposed esophagus that had been connected to a water column of 130 cm height. Slow and fast increases of esophageal pressure were performed and the water pressure at which leakage appeared was registered. RESULTS:The Combitube, Easytube, and intubating laryngeal mask Fastrach withstood the water pressure up to more than 120 cm H2O. The laryngeal mask airway ProSeal, laryngeal tube, and laryngeal tube LTS II were able to block the esophagus until 72–82 cm H2O. The classic laryngeal mask airway showed leakage at 48 cm H2O, but only minor leakage was found in the trachea. Devices with an additional esophageal drain tube drained fluid sufficiently without pulmonary aspiration. CONCLUSIONS:Concerning the risk of aspiration, the use of devices with an additional esophageal drainage lumen might be superior for use in patients with an increased risk of aspiration. The Combitube, Easytube, and intubating laryngeal mask Fastrach showed the best capacity to withstand an increase of esophageal pressure.

Intracellular Ca2+ dependence of nitric oxide mediated enhancement of interleukin-8 secretion in human endothelial cells

Nitric oxide (NO⋅) can induce transient [Ca2+] changes in endothelial cells not different from receptor mediated signalling. Whether this Ca2+ signal may provide a link with IL‐8 secretion induced by NO⋅ donors was investigated in human endothelial cells. Sodium nitroprusside (SNP) and S‐nitroso‐N‐acetyl‐dl‐penicillamine (SNAP) dose dependently increased IL‐8 production in this cell type. Additive IL‐8 secretion was found with TNFα. Buffering intracellular Ca2+ with MAPT/AM suppressed NO⋅ induced [Ca2+]i changes and reduced subsequent IL‐8 secretion. The additive effect of both NO⋅ donors on TNFα induced IL‐8 secretion was completely blocked in the presence of MAPT/AM. SKF 96365, which has been shown to block receptor mediated Ca2+ entry, and TMB‐8, which blocks intracellular Ca2+ release, both inhibited IL‐8 secretion, particularly when TNFα was used as a costimulator, indicating that [Ca2+]i changes are important components of IL‐8 induction by NO⋅.

Schmerztherapie bei elektiven Kolonresektionen – «on-demand», systemische patientenkontrollierte Analgesie oder thorakale Periduralanalgesie?

Für eine schnelle postoperative Rekonvaleszenz und eine hohe Patientenzufriedenheit ist eine adäquate Schmerztherapie eine der wesentlichen Voraussetzungen. Nur durch eine annähernde Schmerzfreiheit nach abdominalchirurgischen Eingriffen ist eine frühe postoperative Mobilisation möglich. Dies ist besonders wichtig für «Fast-track»-Rehabilitationskonzepte, deren Ziel es ist, den Genesungsprozess der Patienten zu beschleunigen, allgemeine Komplikationen zu vermeiden und das Risiko operativer Eingriffe zu vermindern. Durch eine thorakale Periduralanalgesie kann bei Kolonresektionen eine fast vollständige Schmerzfreiheit erzielt werden. Die kombinierte Gabe eines Lokalanästhetikums und eines Opioids in den Periduralraum stellt die effektivste Analgesietechnik bei abdominalchirurgischen Eingriffen dar. Darüber hinaus hat dieses Verfahren einen positiven Einfluss auf die postoperative Funktion des Magen-Darm- Trakts. Die patientenkontrollierte systemische Opioidgabe stellt eine alternative schmerztherapeutische Behandlungsstrategie dar. Allerdings besitzt dieses Verfahren gerade bei abdominalchirurgischen Patienten eine Reihe von Nachteilen. So ist der analgetische Effekt von Opioiden zwar bei ruhenden Patienten hoch, bei rascher postoperativer Mobilisation nimmt die Effektivität der Opioide jedoch deutlich ab. Außerdem hat diese Substanzgruppe einen sedierenden Effekt, wirkt proemetisch und beeinträchtigt die postoperative Darmmotilität. Es hat sich als besonders günstig erwiesen, die thorakale Periduralanalgesie mit der systemischen Gabe von Nichtopioidanalgetika wie Metamizol, Paracetamol oder COX-II-Hemmern zu kombinieren. Die zusätzliche Basisanalgesie durch die Nichtopioidanalgetika ist auch zur Bekämpfung extraabdomineller Schmerzen geeignet.

Relationship between ambient temperature and frequency and severity of cardiovascular emergencies: A prospective observational study based on out-of-hospital care data

OBJECTIVE To test the hypothesis that more cardiovascular emergencies occur at low rather than at high temperatures under moderate climatic conditions. METHODS This was a prospective observational study performed in a prehospital setting. Data from the Emergency Medical Service in Hamburg (Germany) and from the local weather station were evaluated over a 5-year period. Temperature data were matched with the associated rescue mission data. Lowess-Regression analysis was performed to assess the relationship between the temperature and the frequency of individual cardiovascular emergencies. In addition, three threshold-temperatures (0°C, 10°C, 20°C) were defined in order to determine the frequency of cardiovascular emergencies above and below each cut-off value. The severity of emergencies was assessed using the National Advisory Committee for Aeronautics (NACA) scoring system. RESULTS A total of 35,390 cardiovascular emergencies were treated by Emergency Physicians. Transient Loss of Consciousness increased at high temperatures (above 20°C): +43% (95%-CI: [27%; 59%]). In contrast, Coronary Artery Disease +26% (95%-CI: [17%; 34%]), Cardiac Pulmonary Edema +21% (95%-CI: [14%; 27%]), Hypertensive Urgency +18% (95%-CI: [10%; 25%]) and Cerebrovascular Accident +17% (95%-CI: [8%; 24%]) increased at low temperatures, particularly below 10°C (significance level for all: p<0.001). No temperature-related effect was seen in Cardiac Arrhythmia and Pulmonary Embolism and no significant correlation was found between the severity of emergencies and temperature. CONCLUSIONS Our findings suggest that some cardiovascular emergencies such as Coronary Artery Disease, Cardiac Pulmonary Edema, Hypertensive Urgency and Cerebrovascular Accident are more frequent in low temperatures even under mild climatic conditions.

Association between Weather-Related Factors and Cardiac Arrest of Presumed Cardiac Etiology: A Prospective Observational Study Based on Out-of-Hospital Care Data

Abstract Objective: The objective of this study was to determine the association between weather-related factors and out-of-hospital cardiac arrest (OHCA) of presumed cardiac etiology. Methods: This was a prospective observational study performed in a prehospital setting. Data from the Emergency Medical Service in Hamburg (Germany) and data from the local weather station were evaluated over a 5-year period. Weather data (temperature, humidity, air pressure, wind speed) were obtained every minute and matched with the associated rescue mission data. Lowess-Regression analysis was performed to assess the relationship between the above-mentioned weather-related factors and OHCA of presumed cardiac etiology. Additionally, varying measuring-ranges were defined for each weather-related factor in order to compare them with each other with regard to the probability of occurrence of OHCA. Results: During the observation period 1,558 OHCA with presumed cardiac etiology were registered (age: 67 ± 19 yrs; 62% male; hospital admission: 37%; survival to hospital discharge: 6.7%). Compared to moderate temperatures (5 – 25°C), probability of OHCA-occurrence increased significantly at temperatures above 25°C (p = 0.028) and below 5°C p = 0.011). Regarding air humidity, probability of OHCA-occurrence increased below a threshold-value of 75% compared to values above this cut-off (p = 0.006). Decreased probability was seen at moderate atmospheric pressure (1000 hPa – 1020 hPa), whereas increased probability was seen above 1020 hPa (p = 0.023) and below 1000 hPa (p = 0.035). Probability of OHCA-occurrence increased continuously with increasing wind speed (p < 0.001). Conclusions: There are associations between several weather-related factors such as temperature, humidity, air pressure, and wind speed, and occurrence of OHCA of presumed cardiac etiology. Particularly dangerous seem to be cold weather, dry air and strong wind.

Prehospital non-invasive ventilation in acute respiratory failure is justified even if the distance to hospital is short

Aims: Evaluation of the efficacy of prehospital non‐invasive ventilation (NIV) in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD) and cardiogenic pulmonary edema (CPE). Material and methods: Consecutive patients who were prehospitally treated by Emergency Physicians using NIV were prospectively included. A step‐by‐step approach escalating NIV‐application from continuous positive airway pressure (CPAP) to continuous positive airway pressure supplemented by pressure support (CPAP‐ASB) and finally bilevel inspiratory positive airway pressure (BIPAP) was used. Patients were divided into two groups according to the prehospital NIV‐treatment‐time (NIV‐group 1: ≤15 min, NIV‐group 2: >15 min). In addition, a historic control group undergoing standard care was created. Endpoints were heart rate, peripheral oxygen saturation, breathing rate, systolic blood pressure, and a dyspnea score. Results: A total of 99 patients were analyzed (NIV‐group 1: n = 41, NIV‐group 2: n = 58). The control group consisted of 30 patients. The majority of NIV‐patients (90%) received CPAP‐ASB, while CPAP without ASB was conducted in 8% and BIPAP‐ventilation in 2% of all cases. Technical application of NIV lasted 6.1 ± 3.8 min. NIV‐treatment‐time was as follows: NIV‐group 1: 13.1 ± 3.2 min, NIV‐group 2: 22.8 ± 5.9 min. Differences between baseline‐ and hospital admission values of all endpoints showed significantly better improvement in NIV‐groups compared to the control group (p < 0.001). The stabilizing effect of NIV in terms of vital parameters was comparable between both NIV‐groups, independent of the duration of treatment (n.s.). Conclusion: Prehospital NIV‐treatment should be performed in patients with COPD‐exacerbation and CPE, even if the distance between emergency scene and hospital is short.