Herausgabe von CT- und MRT-Aufnahmen im Original zur Prüfung von Schadensersatzansprüchen

Ohne Zusammenfassung     

Gesamtschuldnerausgleich im Arzthaftungsprozess

Abstrakt 1. Für eine gesamtschuldnerische Haftung für den Tod eines Patienten ist es grunds?tzlich ausreichend, wenn beide ?rzte durch ihre jeweiligen Behandlungsfehler nebeneinander kausal für den Tod des Patienten geworden sind. Es ist nicht erforderlich, dass der Zweitbehandler auf Untersuchungsergebnisse des Erstbehandlers zurückgegriffen hat oder in dessen Behandlungst?tigkeit eingebunden gewesen ist. 2. Einem entscheidungserheblichen Beweisantritt ist in Anlehnung an die in § 244 Abs. 3–5 StPO geregelten Gründe zur Ablehnung eines angebotenen Beweises unter Berücksichtigung der Besonderheiten des Zivilprozesses nicht nachzugehen, wenn das angebotene Beweismittel ungeeignet ist. 3. Von einer Ungeeignetheit des Beweismittels ist auszugehen, wenn die Krankenunterlagen als Begutachtungsgrundlage für die Erstellung eines medizinischen Sachverst?ndigengutachtens im Hinblick auf die ?rztliche Schweigepflicht des auf Schadensersatz in Anspruch genommenen Arztes nicht verwertet werden k?nnen. 4. Nach dem Tod eines Patienten sind mit Blick auf die H?chstpers?nlichkeit der Entscheidung über die Entbindung von der Schweigepflicht hierzu nicht die Erben berechtigt; vielmehr ist mangels einer Willens?u?erung des Patienten zu Lebzeiten dessen mutma?licher Wille zu erforschen. Sofern hierfür keine anderen Indizien zur Verfügung stehen, kann der beweisbelasteten Partei die Vorlage einer Schweigepflichtentbindungserkl?rung der Erben des verstorbenen Patienten aufgegeben werden, um so einen Anknüpfungspunkt für einen Rückschluss auf den mutma?lichen Willen des Verstorbenen zu haben. Kann die Kl?gerseite eine solche Schweigepflichtentbindungserkl?rung nicht vorlegen und liegen auch im übrigen keine hinreichenden Anhaltspunkte dafür vor, dass der verstorbene Patient eine Befreiung des beklagten Arztes von der Schweigepflicht gewünscht h?tte, ist die Klage ohne sachliche Prüfung abzuweisen. (Leits?tze des Bearbeiters)     

Exercise-induced left bundle branch block: an infrequent phenomenon: Report of two cases

Exercise-induced left bundle branch block(EI-LBBB)is infrequent phenomenon.We present two patients with angina pectoris who developed EI-LBBB during exercise tolerance test.The first patient with typical angina pectoris had significant obstructive coronary artery disease(CAD)requiring percutaneous coronary intervention of multiple lesions including placement of drug eluting stents.The second patient had atypical chest pain without signs of CAD at all.EI-LBBB occurred at a heart rate of 80 bpm and 141 bpm in the first and second patient,respectively.EI-LBBB remained visible through the test till the recovery period in the first patient at a heart rate of 83 bpm and disappeared at 96bpm in the second patient.Both patients with this infrequent phenomenon are discussed and the literature is reviewed.     

Doppler echocardiography distinguishes between physiologic and pathologic “silent” mitral regurgitation in patients with rheumatic fever

Background: The diagnosis of rheumatic fever is based on physical findings (major) and supporting laboratory evidence (minor) as defined by the Jones criteria. Rheumatic carditis is characterized by auscultation of a mitral regurgitant murmur. Doppler echocardiography, however, may detect mitral regurgitation when there is no murmur (“silent” mitral regurgitation), even in normal individuals. Hypothesis: The hypothesis of this study was that physiologic mitral regurgitation can be differentiated from pathologic “silent” mitral regurgitation by Doppler echocardiography. Methods: The study group consisted of 68 patients (2–27 years) with normal two-dimensional imaging and Doppler evidence of mitral regurgitation but no murmur. Patients with rheumatic fever (n = 37) met Jones criteria (chorea in 20, arthritis in 17). Patients without rheumatic fever (n = 31) were referred for innocent murmur (n = 7), abnormal electrocardiogram (n = 13), and chest pain (n = 11). Echoes were independently reviewed by two cardiologists blinded to the diagnosis. Pathologic mitral regurgitation was defined as meeting the following four criteria: (1) length of color jet > 1 cm, (2) color jet identified in at least two planes, (3) mosaic color jet, and (4) persistence of the jet throughout systole. Jet orientation was also noted. Results: Using the above criteria, there was agreement in echo interpretation of pathologic versus physiologic mitral regurgitation in 67 of 68 patients (interobserver variability of 1.5%). Pathologic regurgitation was found in 25 (68%) patients with rheumatic fever but in only 2 (6.5%) patients without rheumatic fever (p<0.001). The specificity of Doppler for detecting pathologic regurgitation was 94% with a positive predictive value of 93%. The color mitral regurgitant jet was posteriorly directed in all 25 patients with rheumatic fever. Conclusion: Pathologic “silent” mitral regurgitation of rheumatic fever can be distinguished from physiologic mitral regurgitation using strict Doppler criteria, particularly when the jet is directed posteriorly. These data support the use of Doppler echocardiography as a minor criterion for evaluating patients with suspected rheumatic fever.     

Soluble kit receptor in human serum

c-kit encodes the transmembrane receptor tyrosine kinase (Kit) for the recently described ligand stem cell factor (SCF). We have developed an enzyme-linked immunosorbent assay for measuring soluble human Kit and we have used the assay to show high levels of soluble Kit in human serum. The distribution of soluble Kit levels was investigated among 112 normal human serum donors. The mean serum level (+/- SD) was found to be 324 +/- 105 ng/mL with the values falling between 163 ng/mL and 788 ng/mL. No correlation between soluble Kit levels and the sexes or ages of the donors was found. Partial purification using immunoaffinity chromatography allowed us to characterize the soluble Kit from pooled human serum. Antibodies generated to a 497-amino acid recombinant human soluble Kit corresponding to the N-terminal extracellular domain of the receptor recognized the serum-derived soluble Kit by immunoblotting. We found that the serum-derived soluble Kit is glycosylated, with mostly N- linked but also O-linked carbohydrate, and with terminal sialic acid residues. When compared with the recombinant human soluble Kit, the serum-derived material was similar both in size and glycosylation pattern. CNBr cleavage of the isolated serum-derived material followed by amino terminal sequencing confirmed the presence of five peptides expected for the extracellular portion of the Kit molecule. The immunoaffinity purified serum-derived soluble Kit inhibited binding of [125I]SCF to membrane-bound receptor in an in vitro assay. These results indicate that soluble Kit could modulate the activity and functions of SCF in vivo.     

Coronary artery disease in congenital single coronary artery in adults:A Dutch case series

AIM:To assess the current diagnostic and therapeutic management and the clinical implications of congenital single coronary artery(SCA) in adults.METHODS:We identified 15 patients with a SCA detected from four Dutch angiography centers in the period between 2010 and 2013.Symptomatic patients who underwent routine diagnostic coronary angiography(CAG) for suspected coronary artery disease and who incidentally were found to have isolated SCA were analyzed.RESULTS:Fifteen(7 females) with a mean age of 58.5 ± 13.78 years(range 43-86) had a SCA.ConventionalCAG demonstrated congenital isolated SCA originating as a single ostium from the right sinus of Valsalva in 6 patients and originating from the left in 9 patients.Minimal to moderate coronary atherosclerotic changes were found in 4,and severe stenotic lesions in another 4 patients.Seven patients were free of coronary atherosclerosis.Runs of non-sustained ventricular tachycardia were documented in 2 patients,one of whom demonstrated transmural ischemic changes on presentation.Myocardial perfusion scintigraphic evidence of transmural myocardial ischemia was found in 1 patient due to kinking and squeezing of the SCA with an interarterial course between the aorta and pulmonary artery.Multi-slice computed tomography(MSCT) was helpful to delineate the course of the anomalous artery relative to the aorta and pulmonary artery.Percutaneous coronary intervention was successfully performed in 3 patients.Eight patients were managed medically.Arterial bypass graft was performed in 4 patients with the squeezed SCA.CONCLUSION:SCA may be associated with transient transmural myocardial ischemia and aborted sudden death in the absence of coronary atherosclerosis.The availability and sophistication of MSCT facilitates the delineation of the course of a SCA.We present a Dutch case series and review of the literature.     

Human umbilical vein endothelial cells display high-affinity c-kit receptors and produce a soluble form of the c-kit receptor

Stem cell factor (SCF) is a hematopoietic growth factor produced by fibroblasts and endothelial cells that stimulates the growth of primitive hematopoietic cells. SCF triggers cell growth by binding to the c-kit receptor. Because endothelial cells can respond to certain hematopoietic growth factors, we tested human umbilical vein endothelial cells for display of the c-kit receptor and examined the effect of SCF on endothelial cell proliferation, adhesion molecule expression, and production of tissue factor. Quantitative binding experiments with 125I-SCF showed both high-affinity (Kd = 42 pmol/L) and low-affinity (Kd = 1.7 nmol/L) c-kit receptors. There were approximately 1,100 high-affinity c-kit receptors, and 5,400 low- affinity c-kit receptors per endothelial cell. Enzyme immunoassays showed that endothelial cells released soluble c-kit receptor and SCF. The transmembrane form of SCF was detected by indirect immunofluorescence analysis using monoclonal or polyclonal anti-SCF receptor antibodies. The addition of SCF (100 ng/mL) did not alter endothelial cell proliferation over a 7-day period. Similarly, there was no change in the release of tissue factor or expression of inducible endothelial adhesion molecules (intercellular adhesion molecule-1, endothelial-leukocyte adhesion molecule-1, and vascular cell adhesion molecule-1) measured by enzyme-linked immunosorbant assay at 4 and 24 hours after SCF addition. The neutralizing anti-c-kit receptor monoclonal antibody SR-1 blocked binding of 125I-SCF to the c- kit receptor by 98% but did not alter endothelial cell proliferation or adhesion-molecule expression. c-kit receptors were also detected on adult endothelial cells lining small blood vessels in normal human lymph nodes. These data indicate that normal human endothelial cells produce SCF and show high-affinity c-kit receptors that have the capacity to dimerize. The lack of response to exogenous SCF may be because of intracellular activation of the c-kit receptor via autocrine production of SCF. Alternatively, SCF and c-kit may play a role other than stimulation of proliferation, adhesion-molecule display, or tissue factor production by endothelial cells. The production of soluble c-kit receptors by normal human endothelial cells may serve to regulate the bioactivity of SCF within the bone marrow microenvironment.