Zur Haftung des Krankenhauses beim Sturz eines Patienten aus dem Rollstuhl

Abstrakt 1. Es ist Sache des Krankenhaustr?gers, darzulegen und nachzuweisen, dass der Sturz aus einem Rollstuhl nicht auf einem pflichtwidrigen Verhalten der Pflegekr?fte beruht, weil es auch hinsichtlich der Frage der Geeignetheit eines solchen Ger?tes für die Unterbindung von selbst?ndigen Gehversuchen eines Patienten um Risiken aus dem Krankenhausbetrieb geht, die von dem Tr?ger der Klinik und dem dort t?tigen Personal voll beherrscht werden k?nnen. 2. Soweit der Krankenhaustr?ger auf Antrag des Pflegepersonals nicht kurzfristig in der Lage ist, eine Sitzwache zur Vermeidung einer akuten Gef?hrdung des Patienten zur Verfügung zu stellen, handelt es sich um ein Organisationsverschulden, für das er nach x 823 BGB haftet. 3. Der Gesch?digte genügt seiner Darlegungslast sowohl hinsichtlich der objektiven Pflichtverletzung als auch des Verschuldens, indem er vortr?gt, dass er im Gefahrenbereich des Sch?digers aus dem Rollstuhl gestürzt sei. Er muss nicht nachweisen, dass der Unfall auf einem Verschulden des Pflegepersonals oder einem Organisationsverschulden des Krankenhaustr?gers beruht. Vielmehr hat der Sch?diger sich insoweit zu entlasten. (Leits?tze der Bearbeiter)     

Clinical and muscle biopsy findings in malignant hyperthermia susceptibility

Patients (155) were investigated for malignant hyperthermia susceptibility (MHS), by in vitro testing of muscle taken from the vastus medialis muscle. Histopathological and histochemical investigation of muscle was also performed. Ultrastructural investigation was performed in 13 MHS patients; 90% of the patients replied to a questionnaire concerning present or previous neuromuscular symptoms. The majority of MHS and MH negative (MHN) patients had no or only minor histopathological and histochemical abnormalities. Core-targetoid fibres were the only potentially important abnormalities found in MHS patients. There were no differences in neuromuscular symptoms between MHS, MHN and control patients, and most patients in both the MHS and MHN group were normal on clinical examination.     

中国大陆地区妇女骨质疏松筛选工具探讨

目的建立适用于中国大陆地区40岁及以上妇女的骨质疏松（osteoporosis，OP）筛选工具。方法以20～39岁妇女腰椎骨密度的均数和标准差作为参考值计算T—score。以双能X线骨密度仪（dual—energy X—ray absorptiometry，DxA）的测量结果作为金标准，采用二分类的Bayes判别分析，建立判别函数。结果我国大陆地区40岁及以上妇女OP筛选工具（osteoporosis screening tool for Chinese，OSTC）为：体重-2×年龄＋50。判别准则为OSTC〉0为无OP危险性，OSTC≤0为有OP危险性。OSTC的正判率为75．78％，灵敏度为76．8％，特异度为75．1％，Kappa值为0．51（P=0．000），说明OSTC与DXA的判定结果一致性尚可。结论OSTC是一个简便的OP筛选工具。根据年龄、体重两个变量的简单计算，即可对我国大陆地区40岁及以上的妇女进行OP危险性的筛选。但OSTC没有得到外部数据的验证，其优劣还有待进一步评价。     

Effect of cisapride on functional dyspepsia in patients with and without histological gastritis: A double-blind placebo-controlled trial

In the present double-blind placebo-controlled study the effect of cisapride on functional dyspepsia was evaluated in patients with and without histological gastritis. Patients with functional dyspepsia and whose symptoms persisted after a 2 week run-in period with antacid treatment were randomized to receive cisapride (10 mg) or matching placebo three times daily for 4 weeks. Symptoms of epigastric pain, bloating, nausea, belching, early satiety and heartburn were graded on a four-point scale based on patients’ feedback and diary card recording. A global response was also formulated by the investigators. One hundred and four patients entered the study and 76 completed the trial, comprising 36 patients with histological gastritis and 40 patients without gastritis. Symptom scores in both gastritis and non-gastritis groups were significantly improved by both cisapride and placebo; however, the improvement was not statistically different between the two treatment groups. Cisapride produced a good or better global response in 58% of subjects with histological gastritis and in 53% of subjects without gastritis compared with 47% and 52%, respectively, of patients on placebo; this difference was not statistically significant. Gastric histology did not influence the effect of cisapride on the symptoms of functional dyspepsia.     

Prevalence of periodontitis in individuals with human leukocyte antigens (HLA) A9, B15, A2, and B5

Objective

Human leukocyte antigens (HLA) have been associated with periodontitis. Previous studies revealed HLA-A9 and HLA-B15 as potential susceptibility factors, while HLA-A2 and HLA-B5 might have protective effects. The aim of the study was to verify these associations in a group of HLA-typed blood donors with previously unknown periodontal status.

Materials and methods

In four German centers, 140 blood donors with known HLA class I status were enrolled and allocated to the following five groups: HLA-A9 (N = 24), HLA-B15 (N = 20), HLA-A2 (N = 30), HLA-B5 (N = 26), and controls (N = 40). Periodontal examination included the measurement of probing depths (PDs), clinical attachment level (CAL), bleeding on probing (BOP), and community periodontal index of treatment needs (CPITN).

Results

Carriers with HLA-A9 and HLA-B15 had higher values of mean PD (P < 0.0001), CAL (P < 0.0001), and BOP (P < 0.002) as well as sites with PD and CAL with ≥4 and ≥6 mm (P < 0.0003), respectively, than controls. Multiple regression analyses revealed HLA-A9, HLA-B15, and smoking as risk indicators for moderate to severe (CPITN 3–4; odds ratio (OR): 66.7, 15.3, and 5.1) and severe (CPITN 4; OR: 6.6, 7.4, and 3.8) periodontitis. HLA-A2 and HLA-B5 did not show any relevant associations.

Conclusion

The present data support a role of HLA-A9 and HLA-B15 as susceptibility factors for periodontitis, whereas HLA-A2 and HLA-B5 could not be confirmed as resistance factors.

Clinical relevance

Both HLA antigens A9 and B15 are potential candidates for periodontal risk assessment.

     

Platelet coagulation factor Va: the major secretory platelet phosphoprotein

Platelet-derived coagulation factor Va is the primary secreted substrate for a thrombin-stimulation-dependent platelet kinase. Human platelet factor Va, consisting of a molecular weight (M(r)) 105,000 heavy chain and an M(r) 74,000 light chain, incorporates phosphate in at least two sites on the light chain. Phosphorylated factor Va represents 50% of the secreted protein-associated phosphate. This modification occurs exclusively at serine residues and is inhibited by H-7 and staurosporine, which suggests a protein kinase C (PKC)-mediated event. Purified plasma factor V and Va are phosphorylated in the light chain region by rat brain PKC. The activity of platelet factor Va in prothrombinase on platelets is not altered when phosphorylation is inhibited by staurosporine. Plasma-derived factor Va in the presence of thrombin stimulated platelets is phosphorylated on both the heavy chain and the light chain. Plasma factor V and factor Va heavy chain phosphorylation occurs without light chain phosphorylation in the presence of added 32P gamma-ATP and non-stimulated or collagen- stimulated platelets or casein kinase II. This differential phosphorylation of factor Va heavy and light chain shows two independent platelet kinase activities that act on factor Va. The heavy chain factor V/Va kinase activity is similar to casein kinase II, which we have demonstrated previously to act on factor Va and accelerate activated protein C inactivation of the cofactor. Our data show platelet-dependent phosphorylation of platelet and plasma factor V and Va resulting in significant covalent modifications of the cofactor. These modifications may play a role in directing the extracellular distribution of factor V and factor Va.