Das Refeeding-Syndrom ist eine gefährliche, mitunter lebensbedrohliche Komplikation, die nach der Wiederaufnahme einer adäquaten Nahrungszufuhr bei mangelernährten und kachektischen Patienten entstehen kann. Die Entwicklung eines Refeeding-Syndroms wurde nach oraler, enteraler und parenteraler Ernährung beschrieben. Ein frühzeitiges Erkennen eines Refeeding-Syndroms ist für eine adäquate Therapie unumgänglich, jedoch leider aufgrund einer unzureichenden Kenntnis dieses Krankheitsbilds nicht regelhaft. Leitsymptom des Refeeding-Syndroms ist eine Hypophosphatämie. Häufig wird diese von weiteren Elektrolytentgleisungen sowie von Mangelzuständen an Vitaminen und Spurenelementen begleitet. Aufgrund einer Zufuhr an Kohlenhydraten sowie intravenöser Flüssigkeitsgabe kann es zu einer Hypervolämie mit Herzversagen kommen. Weitere Organfunktionsstörungen unterschiedlichen Schweregrads, die bis zum Tod führen können, sind beschrieben worden. Zur Prävention eines Refeeding-Syndroms ist eine frühzeitige Identifikation von Risikopatienten und eine initial niedrige Kalorienzufuhr, begleitet von regelmäßigen laborchemischen Kontrollen unter Nahrungsaufbau, empfehlenswert. Methoden: Literaturrecherche mit den Begriffen „refeeding syndrome“ sowie „hypophosphataemia“ mit Einbeziehung der NICE-Leitlinien aus dem Jahre 2006.
With the establishment of the European Public Prosecutor's Office (EPPO), a quantum leap in cross-border criminal prosecution in Europe has been achieved. One year after the start of operational activities, a conference took place at the University of Munich, which was dedicated to initial experiences, practical problems as well as unresolved scientific questions in connection with the EPPO. The contributions in the accompanying conference proceedings concern the practice of cross-border criminal proceedings, questions of jurisdiction in investigative proceedings, cooperation with national investigative authorities, gathering and utilisation of evidence, as well as the transnationality of criminal prosecution as a challenge for criminal defence.
Established alternative methods of visualisation of intracranial vessels--MR-angiography and angio-CT--give only two dimensional views similar to angiography. It is a subjective matter of the neurosurgeon's imagination to produce three dimensional views on the basis of these methods. Three dimensional processing of dynamic sequence or helical axial computed tomograms give any number you like of stereo-scopic views of the Willisi circulus. Comparing the usefulness of DSA and 3D-CT in 34 aneurysms, the latter often gives supplementary information concerning the direction, neck and adjacent arteries, helpful in planning surgery treatment. It is difficult or sometimes impossible to separate basal aneurysms (a.c.i.) from sinus cavernosus and skull base by this method, but especially in aneurysms located in the area of a.com.a. and c.m.a. the 3D-CT is sufficient for diagnosis and planning surgical treatment without DSA.
1) understand the different patterns of myocardial fibrosis and the degree of isoform-expression and phosphorylation changes in cardiomyocyte titin in the different hemodynamic subgroups of aortic stenosis; 2) examine the extent of myocardial remodeling in paradoxical aortic stenosis to help better understand the poor prognosis of these patients; and 3) review the current guidelines and management of severe aortic stenosis, including evaluation focused on hemodynamic subtypes.
Atrial fibrillation (AF) is associated with thromboembolic events. Currently, the CHA2DS2-VASc score is recommended for thromboembolic risk stratification in non-valvular AF patients. However, recent data suggested a potential role of atrial remodelling on thromboembolism. This study aimed to assess the association between left atrial low-voltage area (LVA) and history of clinical manifest as well as subclinical silent cerebral ischaemia (SCI) in AF patients. Two-hundred patients [64 ± 10.5 years, 75 women (37.5%)] with symptomatic paroxysmal (n = 88, 44%) or persistent AF undergoing pulmonary vein isolation (PVI) were prospectively enrolled. Left atrial LVA (bipolar voltage < 0.5mV) was evaluated by intra-procedural mapping (>300 points per patient) during sinus rhythm. Cerebral delayed-enhancement magnetic resonance imaging was performed after PVI for detection of pre-existing procedural-independent SCI. Over all, 17 patients (8.5%) had previous history of stroke. Pre-existing SCIs were detected in 135 patients (67.5%). Patients with previous stroke (4.0 ± 1.5 vs. 2.1 ± 1.3, P < 0.0001) and pre-existing SCI (2.7 ± 1.3 vs. 1.5 ± 1.4, P < 0.0001) had a significantly higher CHA2DS2-VASc score. LVA was significantly larger in patients with previous stroke (12.5 ± 8.5% vs. 3.4 ± 5.4%, P < 0.0001) as well as pre-existing SCI (5.8 ± 6.9% vs. 0.8 ± 1.7%, P < 0.0001). Multivariate regression analysis revealed that LVA was independently associated with the presence of SCI [hazard ratio (HR) per 1% LVA 1.13 (1.06–1.22), P = 0.0003] and history of stroke [HR per 1% LVA 1.36 (1.19–1.60), P < 0.0001] after adjustment of CHA2DS2-VASc score. Left atrial LVA is associated with history of stroke and SCI in patients with non-valvular AF and might improve thromboembolic risk stratification after confirmation of its predictive value in future studies.
Silent cerebral lesions (SCL) have been identified on magnetic resonance imaging (MRI) in patients after atrial fibrillation (AF) ablation. SCL represent irreversible cerebral damage, comparative a...
Zusammenfassung Hintergrund Chronischer Schmerz ist nach Unfällen und Operationen eine Langzeitkomplikation, deren Relevanz für Patienten im BG-lichen Heilverfahren in Deutschland kaum untersucht ist. Fragestellung Erste Statuserhebung der Häufigkeit chronischer Schmerzen nach Arbeitsunfall. Methoden In 2017 wurden chirurgisch-stationäre BG-Patienten (18–65 J.) eines Tertiärkrankenhauses zu chronischen Schmerzen, die seit einem BG-lich anerkannten Trauma bestanden (Intervall 2,8±6,9 Jahre), ungeachtet einer stattgehabten Versorgung, erstmalig zum Zeitpunkt eines Krankenhausaufenthalts und dann telefonisch 6 Monate später befragt. Der Fokus lag auf Patienten mit einem Arbeitsunfall (A) innerhalb des letzten Monats oder (B) >6 Monaten. Primäres Outcome: Häufigkeit arbeitsunfallbedingter chronischer Schmerzen (>6 Monate) zum Initialinterview (Punktprävalenz), sekundäre Outcomes: Häufigkeit einer Chronifizierung nach 6 Monaten (A) und Persistenz chronischer Schmerzen (B). Tertiäre Outcomes: Arbeitsfähigkeit, Verletzungsartenverfahren, Auswirkungen anhand Schmerzintensität, -lokalisation und -medikation, Funktionseinschränkung in Abhängigkeit der Existenz chronischer Schmerzen sowie Komorbidität. Ergebnisse 415 Patienten wurden eingeschlossen, 85% (160/188) berichteten von unfallabhängigen chronischen Schmerzen (überwiegend mittlere bis sehr starke Intensität, an Gelenken und Knochen lokalisiert). 90% (131/145) gaben diese Schmerzen auch sechs Monate später an. 67% (64/96) gaben erstmalig chronische Schmerzen an. Patienten mit chronischen Schmerzen zum Follow-up (281/369) nahmen seltener ihre Berufstätigkeit wieder auf (p=0,003), in 60% Analgetika ein, waren öfter komorbide (p<0,002) und stärker in ihrer Extremitätenfunktionalität beeinträchtigt (p<0,002). Schlussfolgerung Auch wenn die Ergebnisse als vorläufig zu bewerten sind, scheinen chronische Schmerzen nach Arbeitsunfall sehr häufig und beeinflussen die Wiederherstellung der Arbeitsfähigkeit langfristig negativ. Anhand der vorliegenden anamnestischen Zahlen ist eine weiterführende differenzierte Reevaluation prospektiver Daten unter Beachtung therapeutischer Maßnahmen dringend anzuraten.
Abstract Despite treatment with levothyroxine, hypothyroidism and autoimmune thyroiditis (AIT) may be associated with reduced quality of life (QoL), an enigmatic condition referred to as "syndrome T". Peripheral neuropathy, described in untreated thyroid disease, could be a contributing mechanism. We analysed autonomic and somatosensory function in 29 patients with AIT and treated hypothyroidism and 27 healthy volunteers. They underwent heart rate variability (HRV) analysis and quantitative sensory testing (n = 28), comprising 13 parameters of small and large nerve fibre function and pain thresholds. Autonomic cardiovascular function was assessed in rest, deep respiration and orthostasis. Additionally, biomarkers for autoimmunity and thyroid function were measured. Anxiety, depression and QoL were assessed using validated questionnaires. 36% of the patients showed at least one sign of somatosensory small or large fibre dysfunction. 57% presented with mild hyperalgesia to at least one stimulus. Several markers of autonomic function and some detection thresholds were related to the antibody titres. Anxiety, depression scores and QoL correlated to antibody titres and HRV measures. Autonomic and somatosensory dysfunction indicate that in treated hypothyroidism and AIT a subgroup of patients suffers from neuropathic symptoms leading to impaired QoL. Additionally, mild hyperalgesia as a possible sensitisation phenomenon should be considered a target for symptomatic treatment.
Several influences modulate biochemical responses to a weight-adjusted levothyroxine (l-T4) replacement dose. We conducted a secondary analysis of the relationship of l-T4 dose to TSH and free T3 (FT3), using a prospective observational study examining the interacting equilibria between thyroid parameters. We studied 353 patients on steady-state l-T4 replacement for autoimmune thyroiditis or after surgery for malignant or benign thyroid disease. Peripheral deiodinase activity was calculated as a measure of T4-T3 conversion efficiency. In euthyroid subjects, the median l-T4 dose was 1.3 μg/kg per day (interquartile range (IQR) 0.94,1.60). The dose was independently associated with gender, age, aetiology and deiodinase activity (all P<0.001). Comparable FT3 levels required higher l-T4 doses in the carcinoma group (n=143), even after adjusting for different TSH levels. Euthyroid athyreotic thyroid carcinoma patients (n=50) received 1.57 μg/kg per day l-T4 (IQR 1.40, 1.69), compared to 1.19 μg/kg per day (0.85,1.47) in autoimmune thyroiditis (P<0.01, n=76) and 1.08 μg/kg per day (0.82, 1.44) in patients operated on for benign disease (P< 0.01, n=80). Stratifying patients by deiodinase activity categories of <23, 23-29 and >29 nmol/s revealed an increasing FT3-FT4 dissociation; the poorest converters showed the lowest FT3 levels in spite of the highest dose and circulating FT4 (P<0.001). An l-T4-related FT3-TSH disjoint was also apparent; some patients with fully suppressed TSH failed to raise FT3 above the median level. These findings imply that thyroid hormone conversion efficiency is an important modulator of the biochemical response to l-T4; FT3 measurement may be an additional treatment target; and l-T4 dose escalation may have limited success to raise FT3 appropriately in some cases.
The long-held concept of a proportional negative feedback control between the thyroid and pituitary glands requires reconsideration in the light of more recent studies. Homeostatic equilibria depend on dynamic inter-relationships between thyroid hormones and pituitary thyrotropin (TSH). They display a high degree of individuality, thyroid-state-related hierarchy, and adaptive conditionality. Molecular mechanisms involve multiple feedback loops on several levels of organization, different time scales, and varying conditions of their optimum operation, including a proposed feedforward motif. This supports the concept of a dampened response and multistep regulation, making the interactions between TSH, FT4, and FT3 situational and mathematically more complex. As a homeostatically integrated parameter, TSH becomes neither normatively fixed nor a precise marker of euthyroidism. This is exemplified by the therapeutic situation with L-thyroxine (\(\tiny {L}\)-T4) where TSH levels defined for optimum health may not apply equivalently during treatment. In particular, an FT3–FT4 dissociation, discernible FT3–TSH disjoint, and conversion inefficiency have been recognized in \(\tiny {L}\)-T4-treated athyreotic patients. In addition to regulating T4 production, TSH appears to play an essential role in maintaining T3 homeostasis by directly controlling deiodinase activity. While still allowing for tissue-specific variation, this questions the currently assumed independence of the local T3 supply. Rather it integrates peripheral and central elements into an overarching control system. On \(\tiny {L}\)-T4 treatment, altered equilibria have been shown to give rise to lower circulating FT3 concentrations in the presence of normal serum TSH. While data on T3 in tissues are largely lacking in humans, rodent models suggest that the disequilibria may reflect widespread T3 deficiencies at the tissue level in various organs. As a consequence, the use of TSH, valuable though it is in many situations, should be scaled back to a supporting role that is more representative of its conditional interplay with peripheral thyroid hormones. This reopens the debate on the measurement of free thyroid hormones and encourages the identification of suitable biomarkers. Homeostatic principles conjoin all thyroid parameters into an adaptive context, demanding a more flexible interpretation in the accurate diagnosis and treatment of thyroid dysfunction.
