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  • 1
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    S2k guideline for diving accidents (2023)
    German Medical Science GMS Publishing House; Düsseldorf
    In:  GMS German Medical Science; VOL: 21; DOC01 /20230303/
    Details
    Publication Date: 2023-03-27
    Description: For the purposes of this guideline, a diving accident is defined as an event that is either potentially life-threatening or hazardous to health as a result of a reduction in ambient pressure while diving or in other hyperbaric atmospheres with and without diving equipment. This national consensus-based guideline (development grade S2k) presents the current state of knowledge and recommendations on the diagnosis and treatment of diving accident victims. The treatment of a breath-hold diver as well as children and adolescents does not differ in principle.In this regard only unusual tiredness and itching without visible skin changes are mild symptoms.The key action statements: on-site 100% oxygen first aid treatment, immobilization/no unnecessary movement, fluid administration and telephone consultation with a diving medicine specialist are recommended.Hyperbaric oxygen therapy (HBOT) remains unchanged as the established treatment in severe cases, as there are no therapeutic alternatives. The basic treatment scheme recommended for diving accidents is hyperbaric oxygenation at 280 kPa.
    Description: Ein Tauchunfall im Sinne dieser Leitlinie ist ein potenziell lebensbedrohliches oder gesundheitsschädigendes Ereignis, hervorgerufen durch Abfall des Umgebungsdruckes beim Tauchen oder aus sonstiger hyperbarer Atmosphäre mit und ohne Tauchgerät. Diese nationale S2k-Leitlinie legt den aktuellen Stand der Erkenntnisse und der konsentierten Empfehlungen in der Diagnostik und Behandlung von Patienten nach Tauchunfällen dar. Die Behandlung von Apnoetauchern sowie Kindern und Jugendlichen unterscheidet sich prinzipiell nicht.Milde Symptome sind nur die auffällige Müdigkeit und ein Hautjucken ohne sichtbare Hautveränderungen.Wesentliche Bedeutung bei der Versorgung von Tauchunfällen hat die frühzeitige Atmung von 100%igem Sauerstoff. Weiterhin werden die Ruhiglagerung/keine unnötige Bewegung, eine moderate Flüssigkeitsgabe und eine Taucherärztliche Telefonberatung empfohlen.Die hyperbare Sauerstofftherapie (HBOT) ist bei schweren Dekompressionsunfällen unverändert ohne therapeutische Alternative. Als Behandlungsschema wird grundsätzlich eine HBOT bei 280 kPa empfohlen.
    Subject(s): diving accident ; decompression sickness ; decompression illness ; arterial gas embolism ; oxygen ; hyperbaric oxygen therapy ; Tauchunfall ; Dekompressionserkrankung ; arterielle Gasembolie ; Sauerstoff ; hyperbare Sauerstofftherapie ; ddc: 610
    Language: English
    Type: article
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    GERMAN MEDICAL SCIENCE
  • 2
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    Endonasale mikroskopische Dakryozystorhinostomie - unsere Erfahrung (2008)
    German Medical Science GMS Publishing House; Düsseldorf
    In:  79. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie; 20080430-20080504; Bonn; DOC08hnod414 /20080422/
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    Publication Date: 2008-04-21
    Subject(s): ddc: 610
    Language: German
    Type: conferenceObject
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    GERMAN MEDICAL SCIENCE
  • 3
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    S2k guideline diagnosis and treatment of carbon monoxide poisoning (2021)
    German Medical Science GMS Publishing House; Düsseldorf
    In:  GMS German Medical Science; VOL: 19; DOC13 /20211104/
    Details
    Publication Date: 2021-11-05
    Description: Carbon monoxide (CO) can occur in numerous situations and ambient conditions, such as fire smoke, indoor fireplaces, silos containing large quantities of wood pellets, engine exhaust fumes, and when using hookahs.Symptoms of CO poisoning are nonspecific and can range from dizziness, headache, and angina pectoris to unconsciousness and death.This guideline presents the current state of knowledge and national recommendations on the diagnosis and treatment of patients with CO poisoning.The diagnosis of CO poisoning is based on clinical symptoms and proven or probable exposure to CO. Negative carboxyhemoglobin (COHb) levels should not rule out CO poisoning if the history and symptoms are consistent with this phenomenon. Reduced oxygen-carrying capacity, impairment of the cellular respiratory chain, and immunomodulatory processes may result in myocardial and central nervous tissue damage even after a reduction in COHb.If CO poisoning is suspected, 100% oxygen breathing should be immediately initiated in the prehospital setting.Clinical symptoms do not correlate with COHb elimination from the blood; therefore, COHb monitoring alone is unsuitable for treatment management. Especially in the absence of improvement despite treatment, a reevaluation for other possible differential diagnoses ought to be performed.Evidence regarding the benefit of hyperbaric oxygen therapy (HBOT) is scant and the subject of controversy due to the heterogeneity of studies.If required, HBOT should be initiated within 6 h.All patients with CO poisoning should be informed about the risk of delayed neurological sequelae (DNS).
    Description: Kohlenmonoxid (CO) kann in zahlreichen Situationen und Umgebungen auftreten, beispielsweise Brandrauch, Feuerstellen in geschlossenen Räumen, Silos mit großen Mengen an Holzpellets; Motoren-Abgase und der Gebrauch von Wasserpfeifen.Die Symptome einer Kohlenmonoxidvergiftung sind unspezifisch und können Schwindel, Kopfschmerz, Angina pectoris bis zu Bewusstlosigkeit und Tod umfassen.Diese Leitlinie legt den aktuellen Stand der Erkenntnisse und der nationalen Empfehlungen in der Diagnostik und Behandlung von Patienten mit Kohlenmonoxidvergiftungen dar.Die Diagnose einer Kohlenmonoxidvergiftung erfordert klinische Symptome und eine nachgewiesene oder wahrscheinliche Exposition mit Kohlenmonoxid. Ein negativer CO-Hämoglobin (Hb)-Nachweis soll nicht zum Ausschluss einer Kohlenmonoxidvergiftung führen, wenn Anamnese und Symptome übereinstimmend sind. Durch eine reduzierte Sauerstofftransportkapazität, die Beeinträchtigung der zellulären Atmungskette und immunmodulatorische Prozesse kann es auch nach Reduktion des CO-Hb zu myokardialen und zentralnervösen Gewebeschäden kommen.Bei Verdacht auf eine Kohlenmonoxidvergiftung soll präklinisch sofort mit einer 100% Sauerstoffatmung begonnen werden.Die klinische Symptomatik der Patienten korreliert nicht mit der CO-Hb Clearance aus dem Blut. CO-Hb-Kontrollen allein sind für eine Therapiesteuerung ungeeignet. Insbesondere bei fehlender Besserung unter Therapie sollte eine Reevaluation für andere möglicherweise vorliegende Differentialdiagnosen erfolgen.Die Evidenz zum Nutzen der hyperbaren Sauerstofftherapie (HBOT) ist aufgrund der heterogenen Studienlage niedrig und wird kontrovers diskutiert.Der Beginn einer HBOT soll gegebenenfalls innerhalb von 6 Stunden erfolgen.Jeder Patient mit Kohlenmonoxidvergiftung soll über das Risiko eines verzögert einsetzenden neurologischen Defizites (delayed neurological sequelae, DNS), aufgeklärt werden.
    Subject(s): carbon monoxide poisoning ; etiology ; prevention ; prehospital management ; oxygen breathing ; initial in-hospital care ; hyperbaric oxygen therapy ; HBOT ; CO hemoglobin ; delayed neurological sequelae (DNS) ; rehabilitation ; Kohlenmonoxidvergiftung ; Ätiologie ; Prävention ; Primärversorgung ; Sauerstoffatmung ; klinische Erstversorgung ; Hyperbare Sauerstofftherapie ; HBOT ; CO-Hämoglobin ; neurologische Spätschäden (delayed neurological sequelae, DNS) ; Rehabilitation ; ddc: 610
    Language: English
    Type: article
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    GERMAN MEDICAL SCIENCE
  • 4
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    Effects of varying shear stress profiles on the regulation of pulmonary artery endothelial cell gene expression: a focus on selected mediators of vascular tone, inflammation and angiogenesis (2021)
    Oxford University Press
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    Publication Date: 2021-10-01
    Description: Background Pulmonary arterial hypertension (PAH) is a complex pathology characterized by obliterative vascular remodeling that leads to right heart failure and death. Predisposition to PAH is associated with mutations in the BMPR2 gene in approximately 70–80% of familial cases and around 30% for that of sporadic PAH. The study of the pathogenetic basis of PAH is often performed in static endothelial cultures. Such two-dimensional, isolated cell microenvironments fail to consider the heterogeneity in mechanical stress acting on endothelial cells in various regions of the pulmonary vascular tree. In the remodeled pulmonary vasculature, low and oscillatory shear stress is observed in the proximal pulmonary artery with high shear stress in distal pre-capillary pulmonary arterioles. Therefore, the impact of varied shear profiles (including both laminar and oscillatory flow) on pulmonary artery endothelial cell (and that of BMPR2-deplete) gene expression of common vasoactive (EDN1, ENOS), proinflammatory (IL6, IL8) and angiogenic mediators (ANG2, VEGFA), are poorly described. Purpose To evaluate the effects of shear stress magnitude, including unidirectional and oscillatory flow on BMPR2-knockdown human pulmonary artery endothelial cell (HPAEC) gene expression of EDN1, ENOS, IL6, IL8, ANG2 and VEGFA. Methods HPAECs were transfected with siRNA directed against BMPR2 (siB2) or with a non-targeting control (siCon). Cells were exposed to 10 hours of laminar or oscillatory flow (1Hz; 1.5 dyn/cm2, 15 dyn/cm2 or 90 dyn/cm2) using a parallel-plate fluid flow chamber system. Measurement of mRNA expression was performed using qPCR. Results Shear stress intensity and flow type (unidirectional and oscillatory) mediated diverse effects on HPAEC gene expression across the markers studied. Changes in gene expression were calculated relative to that of static siCon-transfected HPAECs and in such a manner are summarized as fold changes in the table below. Asterisks are shown where significant fold differences are reported. *P≤0.05, **P≤0.01, ***P≤0.001, ****P≤0.0001. aP≤0.05, bP≤0.05, cP≤0.05, denote comparisons between groups. Of note, no significant differences in gene expression were observed between static siCon and static siB2. Conclusions For the markers studied, different magnitudes of shear stress and flow profiles (together with BMPR2 loss) exhibit varied patterns of gene expression in the pulmonary vascular endothelium. As such, this illustrates the need for wider study of in vitro endothelial-shear stress interactions in understanding mechanisms of remodeling in PAH. FUNDunding Acknowledgement Type of funding sources: None. Table 1
    Print ISSN: 0195-668X
    Electronic ISSN: 1522-9645
    Topics: Medicine
    Published by Oxford University Press on behalf of European Society of Cardiology.
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  • 5
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    Moving shear stress towards the clinic: preclinical comparison of optical coherence tomography-based versus angiography-based time-averaged wall shear stress estimations (2021)
    Oxford University Press
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    Publication Date: 2021-10-01
    Description: Introduction Identification of coronary atherosclerotic plaques at risk of causing future acute coronary syndromes remains a major unmet clinical challenge. The addition of vessel biomechanics to intracoronary imaging derived evaluation of plaque morphology, improves identification of plaques likely to develop high risk features. We and others have developed a framework for intracoronary imaging (optical coherence tomography [OCT]) based 3D reconstructions of coronary arteries for computational fluid dynamics (CFD) simulations of shear stress, which are considered the current gold standard approach for quantification of coronary arterial haemodynamics. However, these approaches are time consuming and computationally intensive, resulting in a barrier to clinical uptake. Purpose Determination of time averaged wall shear stress (TAWSS) based on 3D coronary geometries from non-invasive 3D Quantitative Coronary Angiography (3D-QCA) has recently been developed (Pie Medical Imaging, Netherlands), which enables results of shear stress simulations to be available within 30 minutes. We sought to compare TAWSS determined from 3D-QCA with gold standard OCT-based CFD simulations in both normal and stenotic arteries in minipigs. Methods 15 normal and 5 stenotic minipig coronary arteries were studied. Anatomically matched 3D arterial geometries were reconstructed from 3D-QCA and OCT using common centrelines. Boundary conditions for simulations included directly measured inlet blood velocities; parabolic inlet flow profiles, zero pressure outlet; no-slip arterial walls; blood density: 1.05 g/ml; blood dynamic viscosity: 0.035 g/cm.s. Blood was modelled as Newtonian. 3D-QCA TAWSS was obtained with a Kratos Multi-Physics CFD solver. OCT-based simulations were performed using Abaqus/CFD v6.14. TAWSS was calculated for 80 axially matched segments for both methods (1200 and 400 paired comparisons for normal and stenotic arteries, respectively). Data were analysed using Bland-Altman and Wilcoxon matched-pairs signed ranked tests. Results Computation times for 3D-QCA and OCT-based CFD were approximately 30 minutes and 2 hours respectively. Axial profiles of TAWSS were similar between the two methods and there was agreement in TAWSS magnitudes and narrow 95% limits of agreement (Figure 1 and Figure 2). Using co-registered TAWSS maps generated by each method, we find similar spatial regional distributions of TAWSS in both normal and stenotic arteries. Conclusions Our data suggest that 3D-QCA based TAWSS is feasible in both normal and stenotic arteries. Spatial TAWSS distributions between the two methods are similar with agreement in matched TAWSS comparisons, though there are some small systematic differences in the absolute values of TAWSS, due to different resultant arterial geometries. These encouraging data suggest that further clinical evaluation of rapid TAWSS from 3D-QCA is warranted, which may facilitate clinical adoption of TAWSS assessment. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – EU funding. Main funding source(s): Medical Research Council
    Print ISSN: 0195-668X
    Electronic ISSN: 1522-9645
    Topics: Medicine
    Published by Oxford University Press on behalf of European Society of Cardiology.
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