Beobachtungen zur ?rztlichen übergabe auf der Intensivstation – ein Qualit?tsmanagementprojekt

Introduction

In medicine and especially in intensive care, errors lead to significant consequences especially due to the limited time and resources environment. The range of errors is wide, but a major portion is referred to “information loss” or “information degrading”. Therefore, we conducted a quality assurance audit to evaluate medical shift changes in the intensive care unit.

Methods

We analyzed the doctor’s shift change and sharing of information in a medical 12-bed ICU in a university hospital. The questionnaire was given to the physicians and a video documentation of the actual shift change was recorded. We compared the results of the audit before and after a switch from an 8-hour shift to a 12-hour shift a year later.

Results

A 60-minute shift change (for an average of 10 patients) was regarded sufficient. The sharing of information should be performed at the bed side or in front of the room/slot. Critical loss of information was not noted in this evaluation. Passing on social context information and the rationale for therapy changes were not regarded as important. We observed many disruptions during the shift change; combining the shift change with a regular ward round was not regarded useful.

Consequences

Shift changes in our institution are not conducted in a straightforward fashion. Loss of critical information was not observed. More detailed investigations to optimize medical shift changes are warranted.     

Antiviral effects of a probiotic Enterococcus faecium strain against transmissible gastroenteritis coronavirus

The enteropathogenic coronavirus transmissible gastroenteritis virus (TGEV) causes severe disease in young piglets. We have studied the protective effects of the probiotic Enterococcus faecium NCIMB 10415 (E. faecium), which is approved as a feed additive in the European Union, against TGEV infection. E. faecium was added to swine testicle (ST) cells before, concomitantly with, or after TGEV infection. Viability assays revealed that E. faecium led to a dose-dependent rescue of viability of TGEV-infected cells reaching nearly to complete protection. Virus yields of the E. faecium–treated cultures were reduced by up to three log₁₀ units. Western blot analysis of purified TGEV revealed that the levels of all viral structural proteins were reduced after E. faecium treatment. Using transmission electron microscopy, we observed attachment of TGEV particles to the surface of E. faecium which might be a means to trap virus and to prevent infection. Increased production of nitric oxide in the cells treated with E. faecium and elevated expression of interleukin 6 and 8 pointed to stimulated cellular defense as a mechanism to fight TGEV infection.     

Mucosal melanomas of different anatomic sites share a common global DNA methylation profile with cutaneous melanoma but show location-dependent patterns of genetic and epigenetic alterations

Cutaneous, ocular, and mucosal melanomas are histologically indistinguishable tumors that are driven by a different spectrum of genetic alterations. With current methods, identification of the site of origin of a melanoma metastasis is challenging. DNA methylation profiling has shown promise for the identification of the site of tumor origin in various settings. Here we explore the DNA methylation landscape of melanomas from different sites and analyze if different melanoma origins can be distinguished by their epigenetic profile. We performed DNA methylation analysis, next generation DNA panel sequencing, and copy number analysis of 82 non-cutaneous and 25 cutaneous melanoma samples. We further analyzed eight normal melanocyte cell culture preparations. DNA methylation analysis separated uveal melanomas from melanomas of other primary sites. Mucosal, conjunctival, and cutaneous melanomas shared a common global DNA methylation profile. Still, we observed location-dependent DNA methylation differences in cancer-related genes, such as low frequencies of RARB (7/63) and CDKN2A promoter methylation (6/63) in mucosal melanomas, or a high frequency of APC promoter methylation in conjunctival melanomas (6/9). Furthermore, all investigated melanomas of the paranasal sinus showed loss of PTEN expression (9/9), mainly caused by promoter methylation. This was less frequently seen in melanomas of other sites (24/98). Copy number analysis revealed recurrent amplifications in mucosal melanomas, including chromosomes 4q, 5p, 11q and 12q. Most melanomas of the oral cavity showed gains of chromosome 5p with TERT amplification (8/10), while 11q amplifications were enriched in melanomas of the nasal cavity (7/16). In summary, mucosal, conjunctival, and cutaneous melanomas show a surprisingly similar global DNA methylation profile and identification of the site of origin by DNA methylation testing is likely not feasible. Still, our study demonstrates tumor location-dependent differences of promoter methylation frequencies in specific cancer-related genes together with tumor site-specific enrichment for specific chromosomal changes and genetic mutations. © 2021 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland.     

Über hereditären Parkinsonismus

Zusammenfassung Abgesehen von den Parkinsonbildern exogener Genese gibt es mit Bestimmtheit eine Gruppe hereditären Parkinsonismus, für die am besten die Bezeichnung Paralysis agitans reserviert bliebe. An Hand der Beschreibung mehrerer Fälle werden Parkinsonsymptome in 4 aufeinanderfolgenden Generationen nachgewiesen, und zwar stets von Mutter auf Tochter und deren Besonderheiten ausgeführt. Es wird eine spezielle Psychopathie als jahrzehntelanges Prodromalstadium beschrieben, die insbesondere bei der Probandin, die der 3. Generation angehört, zu beobachten ist. Die psychische Enthemmung wird als Folge einer Diskordanz zwischen Cortex und Subcortex aufgefaßt, die flüchtigen psychotischen Erscheinungen werden als leichte Bewußtseinsstörungen angesehen. Nach allem besteht zweifellos eine schwere familiäre Entartung mit phyletischer Symptomanreicherung besonders auf psychischem Gebiet. Die Möglichkeit der Entwicklung heredodegenerativer Erkrankungen wird erörtert, und insbesondere auf Konsanguinität und gleichförmige Belastung mit Arteriosklerose hingewiesen. Das Vorkommen anderer Erbkrankheiten in der weiteren Familie läßt an eine allen Erberkrankungen zugrunde liegende gleichartige Ursache denken, die allerdings besondere Manifestationen zuläßt, die sich dann nach bestimmtem Modus weiter vererben. Der vonKehrer als dominant vermutete Erbgang der hereditären Paralysis agitans erhält durch das vorliegende Beweismaterial eine eindeutige Stütze. Bei der geringen Zahl eindeutig geklärter Fälle ist die Frage eines Eingriffs im Sinne des Gesetzes vom 14. Juli 1933 bei hereditär parkinsonkranken Familien nicht spruchreif.     

Identification of venous variants in the pineal region with 3D preoperative computed tomography and magnetic resonance imaging navigation. A statistical study of venous anatomy in living patients

OBJECT: The purpose of this study was to determine the ability of software-assisted 3D reconstruction performed using a neuronavigation system to delineate the anatomy and variation patterns of the pineal region venous complex, and then to compare these data with previous anatomical findings. METHODS: The authors retrospectively reviewed the neuroimages obtained in 100 patients with intracranial lesions (50 computed tomography [CT] scans obtained with contrast agents and 50 magnetic resonance [MR] images obtained with gadolinium) by using a neuronavigation workstation for 3D reconstruction. Particular attention was given to the internal cerebral vein, basal vein (BV), and the vein of Galen. The various connection patterns between the major vessels were classified and statistically analyzed. CONCLUSIONS: The venous system of the pineal region shows a wide range of sex-related variations. In the female patient the absence of a BV (Type 0) is significantly more frequent than in the male. In this study the authors illustrate the ability to depict the venous drainage patterns in the pineal region for all cases studied by using 3D neuronavigation software without the need for additional examinations. This simple tool provides important information for surgical planning and may be of significant help intraoperatively.     

Frequent BRAF Gain in Low‐Grade Diffuse Gliomas with 1p/19q Loss

Chromosomal 7q34 duplication and BRAF‐KIAA1549 fusion is a characteristic genetic alteration in pilocytic astrocytomas. 7q34 gain appears to be common in diffuse astrocytomas, but its significance is unclear. We assessed BRAF gain and BRAF mutations in 123 low‐grade diffuse gliomas, including 55 diffuse astrocytomas, 18 oligoastrocytomas and 50 oligodendrogliomas. Quantitative polymerase chain reaction (PCR) revealed BRAF gain in 17/50 (34%) oligodendrogliomas, a significantly higher frequency than in diffuse astrocytomas (7/55; 13%; P = 0.0112). BRAF gain was common in low‐grade diffuse gliomas with 1p/19q loss (39%) and those lacking any of the genetic alterations analyzed (31%), but was rare in those with TP53 mutations (2%). Logistic regression analysis showed a significant positive association between 1p/19q loss and BRAF gain (P = 0.0032) and a significant negative association between TP53 mutations and BRAF gain (P = 0.0042). Fluorescence in situ hybridization (FISH) analysis of 26 low‐grade diffuse gliomas with BRAF gain additionally revealed BRAF‐KIAA1549 fusion in one oligodendroglioma. Sequencing of cDNA in 17 low‐grade diffuse gliomas showed BRAF‐KIAA1549 fusion in another oligodendroglioma. A BRAF^V600E mutation was also detected in one oligodendroglioma, and a BRAF^A598V in one diffuse astrocytoma. These results suggest that low‐grade diffuse gliomas with 1p/19q loss have frequent BRAF gains, and a small fraction of oligodendrogliomas may show BRAF‐KIAA1549 fusion.     

Myofibrillar disorganization characterizes myopathy of camptocormia in Parkinson’s disease

Camptocormia is a highly disabling syndrome that occurs in various diseases but is particularly associated with Parkinson’s disease (PD). Although first described nearly 200 years ago, the morphological changes associated with camptocormia are still under debate and the pathophysiology is unknown. We analyzed paraspinal muscle biopsies of 14 PD patients with camptocormia and compared the findings to sex-matched postmortem controls of comparable age to exclude biopsy site-specific changes. Camptocormia in PD showed a consistent lesion pattern composed of myopathic changes with type-1 fiber hypertrophy, loss of type-2 fibers, loss of oxidative enzyme activity, and acid phosphatase reactivity of lesions. Ultrastructurally, myofibrillar disorganization and Z-band streaming up to electron-dense patches/plaques were seen in the lesions. No aberrant protein aggregation, signs of myositis or mitochondriopathy were found, but the mitochondrial content of paraspinal muscles in patients and controls was markedly higher than known from limb biopsies. Additionally, we were able to demonstrate a link between the severity of the clinical syndrome and the degree of the myopathic changes. Because of the consistent lesion pattern, we propose criteria for the diagnosis of camptocormia in PD from muscle biopsies. The morphological changes show obvious parallels to the muscle pathology of experimental tenotomy reported in the 1970s, which depend on an intact innervation and do not occur after interruption of the myotactic reflexes. A dysregulation of the proprioception could be part of the pathogenesis of camptocormia in Parkinson’s disease, particularly in view of the clinical symptoms of rigidity and loss of muscle strength.