Herzgefäss Medizin Klinik Im Park

IntroductionPrecautions for implanting cardiac implantable electronic devices (CIED) into patients with end-stage kidney disease (ESKD) are more prevalent nowadays. However, concerns about haemodialysis in patients with CIED are rare.Case PresentationA 45-year-old woman with underlying type 2 diabetes mellitus hypertension. She was diagnosed with a complete heart block, which required a permanent pacemaker in 2007, and underwent a box change in 2017. She was further complicated with ESKD, requiring regular peritoneal dialysis since 2019. Unfortunately, she had to convert to haemodialysis in May 2024 due to recurrent peritonitis. The nephrology team referred us as the patient had been oxygen-dependent since starting haemodialysis through internal jugular catheter insertion. Upon review, she had right ventricular failure: oedematous over her lower extremities and had sacral oedema and ascites; a chest drain was inserted for persistent pleural effusion. A loud systolic murmur was heard over the left sternal edge with loud P2. Electrocardiogram shows RV strain pattern. Echocardiography revealed severe tricuspid regurgitation (TR) with a systolic pressure gradient of 80mmHg. 3D echocardiography showed pacemaker wire impinging septal leaflet, causing mechanical TR. Pacemaker interrogation found 99.9% ventricular pacing. Consensus between managing teams and patients was made, and volume control was decided through fluid restriction and haemodialysis to maintain ideal dry weight as guided by a body composition monitor. She eventually developed a hospital-acquired infection, worsening pulmonary hypertension, leading to her demise within 3 months of haemodialysis.DiscussionPatients with ESKD have shorter lives compared to the healthy population. A study found higher mortality in the first 5 months for those with peritoneal dialysis switching over to haemodialysis. Our patient developed severe TR and right ventricular failure after starting with haemodialysis through the internal jugular catheter, with echocardiography evidence of pacemaker wire causing mechanical free flow TR. She was, unfortunately, pacemaker dependent. Transvenous lead retraction and any form of tricuspid valve intervention (surgery / transcatheter edge-to-edge repair / transcatheter tricuspid valve transplant) were too invasive or expensive treatment for her.ConclusionHaemodialysis in ESRD patients may worsen underlying CIED-related TR and is expensive to treat. Serial TR assessment in CIED patients is essential.

Abstract Deep dry needling of post-stroke patients during early rehabilitation has not been applied and documented until now. The present study deals with the first documented case. The effect of deep dry needling (DDN) interventions on hypertension was investigated for a 48-year-old male patient who suffered from brain hemorrhage. It appeared that the DDN-induced temporarily improved ROM facilitated treatment and allowed the patient to exercise in a better alignment and more effectively during treatment. This finding, which should still be validated by more cases, promises to open new perspectives for more effective and shorter-duration treatment of post-stroke patients with spasticity or hypertension.

Differences in epaAC© in heart failure patients with or without readmission: A retrospective case-control study Abstract. Background: Heart failure is one of the most frequent reasons for hospitalization in elderly people. In heart failure, approximately 22.8 % of hospitalised patients are rehospitalised within 30 days. The nursing assessment tool epaAC could provide information on risk factors for readmission. Aim: The aim of this study was to identify possible group differences in the items and scores of the epaAC discharge assessment with regard to the endpoint of unplanned readmissions within 30 days after discharge from index-hospitalisation. Methods: Using a retrospective case-control design, differences in the epaAC variables were investigated by descriptive and comparative statistics. Chi-square test, Wilcoxon test and t-test were performed with two-sided alpha level α < 0.05. Alpha error accumulation was accounted for by Benjamini & Hochberg correction. Results: No significant group differences were found in all items and scores of the discharge epaAC. There is only weak evidence that the presence of acute respiratory impairment at time of discharge is higher in the patient with rehospitalisation than in those without rehospitalisation. Conclusions: The items and scores of the nursing assessment instrument epaAC did not significantly differ between patients with or without 30-days readmission. Further exploration to assess the epaAC's potential to predict rehospitalisation in heart failure is needed.

Die Panarteriitis nodosa wurde von Kussmaul und Maier 1866 beschrieben und damals Periarteriitis nodosa genannt aufgrund der vielen kleinen Knotchen, die entlang einer muskularen Arterie zu finden sind. Als man die wahre Natur der Knotchen erkannte, wurde die Krankheit in Pan- oder Polyarteriitis nodosa (PAN) umbenannt. Es handelt sich um eine nekrotisierende Arteriitis, die kleine und mittelgrose Arterien der meisten Organe befallen kann. Typischerweise sind die Nieren und Viszeralarterien betroffen. Bei der klassischen PAN sind die Pulmonalarterien nicht mitbetroffen, Bronchialgefase konnen aber beteiligt sein.

Leg ulcers (ulcus cruris): The frequent macrovascular causes Abstract. Four pathologies make up the macrovascular etiologies of leg uclers: Venous leg ulcers (50 %), mixed venous-arterial leg ulcers (20 %), arterial leg ulcers (5 %), and Martorell hypertensive ischemic leg ulcer (5 %). The remaining 20 % concern a large array of other etiologies. Every leg ulcer requires vascular (arterial and venous) work-up, that can be completed with microbiology, biopsy, and more in-depth internal diagnostics, as indicated. Venous leg ulcers are treated with compression therapy. Incompetent saphenous veins and tributaries are abolished if the deep venous system is patent. Occluded iliac veins are recanalised and stented, as possible. Refractory venous leg ulcers are grafted with split skin or punch grafts, depending on their surface. Extensive dermatolipofasciosclerosis may be tangentially removed by shave therapy or fasciectomy, that can be combined with negative pressure wound treatment (NPWT). Skin equivalents are an alternative to treat superficial venous leg ulcers that fail to epithelialise. Their indication in the treatment of more complex leg ulcers still needs to be better investigated and understood. The use of dermal matrices leads to more stable scars. Mixed venous-arterial leg ulcers heal slower and recur more frequently. Compression needs to be reduced. Refractory cases require arterial revascularisation, to transform the mixed venous-arterial into a venous leg ulcer. Arterial leg ulcers require arterial revascularization and split skin graft. Martorell hypertensive ischemic leg ulcer is still underrecognised and often confounded with with pyoderma gangrenosum, which leads therapy into a wrong direction. Necrosectomy, antibiotic treatment in the presence of relevant bacterial superinfection, and repeated split skin grafts eventually heal the vast majority of these extremely painful and potentially mortal wounds.

CME-Sonografie 67/Auflösung: AbdominalschmerzenKathrin Müller, Jan Schmidt, and Jan TumaKathrin MüllerInstitut für Sonographie, UsterSearch for more papers by this author, Jan SchmidtChirurgisches Zentrum Zürich, Standort Klinik Im ParkSearch for more papers by this author, and Jan TumaInstitut für Sonographie, UsterSearch for more papers by this authorPublished OnlineDecember 09, 2015https://doi.org/10.1024/1661-8157/a002217PDF ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinkedInReddit SectionsMoreFiguresReferencesRelatedDetails Volume 104Issue 25Dezember 2015ISSN: 1661-8157eISSN: 1661-8165 tabs.informationPraxis (2015), 104, pp. 1414-1416 https://doi.org/10.1024/1661-8157/a002217.© 2015Hogrefe AGPDF download

Das Marfan-Syndrom ist die häufigste angeborene Bindegewebserkrankung. Ursache sind Mutationen im FBN1-Gen, das für Fibrillin-1 kodiert, einen Bestandteil der Mikrofibrillen, die die elastischen Fasern des Bindegewebes bilden. Da elastische Fasern ubiquitär im Körper vorkommen, kann das Marfan-Syndrom mehrere Organe betreffen.