Geriatrische Patientinnen mit Harninkontinenz-Symptomen und ihre Kontrolle über den Beckenboden

Not only do anatomy and function of the pelvic floor play an important role as possible causes of female urinary incontinence, they are also crucial for its therapy. The aim of this case control study of female geriatric patients with symptoms of urinary incontinence was to determine the knowledge about their pelvic floor and to assess their ability to contract pelvic floor muscles voluntarily and reflexly. METHODS: A total of 377 female geriatric patients with symptoms of urinary incontinence were investigated in a Basis Assessment for Urinary incontinence. The ability to contract their pelvic floor muscles was examined by a digital vaginal palpation. The extent of the registered muscle strength was graded by the Modified Oxford Grading Scale by Laycock (1994). RESULTS: Of the patients, 65.5% were not aware of their pelvic floor and were not able to contract the pelvic floor muscles (Grade 0 to 1 by Laycock), 22% had an inaccurate knowledge and only performed an insufficient pelvic floor muscle contraction (Grade 2 by Laycock). Only 12.5% could contract their pelvic floor muscles properly (Grade 3 to 4 by Laycock). A subgroup of 83 patients had already absolved pelvic floor exercises in the past, 80 patients with conventional instructions, 3 patients with digital vaginal control. In this subgroup 54.2% of the patients were not able to contract the pelvic floor muscles (Grade 0 to 1 by Laycock) 25.3% only performed an insufficient contraction (Grade 2 by Laycock), while 20% were able to perform a sufficient and powerful contraction (Grade 3 to 4 by Laycock). The three patients in the past controlled by a digital vaginal palpation were part of this group and managed a pelvic floor muscle strength Grade 4 by Laycock. A high percentage of female geriatric patients with symptoms of urinary incontinence have a lack of understanding regarding the position and function of their pelvic floor. These results suggest that conventional pelvic floor muscle exercises without specific control are not an appropriate method to improve geriatric patients' ability to contract their pelvic floor muscles and to prevent urine leakage.     

Wie sollen Urologen ven?se subkutane Portsysteme implantieren?

Background

Since 1999 urologists at the University of Essen in Germany have performed subcutaneous implantation of venous port systems, controlled by intravasal ECG.

Methods

Between December 1999 and June 2011 implantation of venous port systems was performed in 241 male (69.5%) and 106 (30.5%) female patients. The port systems were implanted subcutaneously above the pectoralis major muscle under local anesthesia. If it was not possible to isolate the cephalic vein or safe catheter implantation was not feasible, puncture of the subclavian vein was performed.

Results

The median follow-up was 491.6 days (2?C2568), and 163.254 catheter days (mean 239 days, range 2?C2604) were documented. During the follow-up period 191 (55.1%) patients died. The mean surgical implantation and explantation time was 36.5 min (14?C85 min) and 25.4 min (10-46 min), respectively; 79.7% were implanted and controlled by ECG. Altogether, 390 devices were used in 379 surgical procedures, 355 implantations (91.1%) and 35 explantations (8.9%). Implanted vessels were the cephalic vein in 303 patients (85.6%) and the subclavian vein in 51 (14.4%) patients. Of 35 explanted devices, the explantation was necessary due to complications in 28 (8.0%) cases: infection n=6 (1.7%, 0.036 per 1,000 catheter days), occlusion n=8 (2.3%, 0.049 per 1,000 catheter days), dislocation n=7 (2.0%, 0.042 per 1,000 catheter days), deep vein thrombosis of the upper extremity n=6 (1.7%, 0.037 per 1,000 catheter days), and clotting n=1(0.3%, 0.006 per 1,000 catheter days). Premature catheter removal (<30?days post-op) was required in six cases (1.9%, 0.036 per 1,000 catheter days) due to complications: three catheter dislocations/malfunctions (0.9%, 0.019 per 1,000 catheter days), one port-related infection, one pocket port infection, and one deep vein thrombosis of the upper extremity (0.3%, 0.006 per 1,000 catheter days). Other problems described in the literature like pneumothorax, vein perforation, or pinch-off syndrome did not occur.

Conclusions

Implantation of port systems with ECG control of the catheter tip position is related to a few cases of adverse events and good surgical outcomes. Furthermore, it has also shown great advantages in offering immediate support and early therapy initiation with a fast learning curve for the training urologists. The results of the presented analysis are comparable to those of surgical or radiological departments reported in the literature and provide good evidence that this procedure should be extended to urological centers with a high volume of chemotherapy patients.     

Inhibition of Gene Expression of Carnitine Palmitoyltransferase I and Heart Fatty Acid Binding Protein in Cyclophosphamide and Ifosfamide-Induced Acute Cardiotoxic Rat Models

This study investigated whether cyclophosphamide (CP) and ifosfamide (IFO) therapy alters the expression of the key genes engaged in long-chain fatty acid (LCFA) oxidation outside rat heart mitochondria, and if so, whether these alterations should be viewed as a mechanism during CP- and IFO-induced cardiotoxicity. Adult male Wistar albino rats were assigned to one of the six treatment groups: Rats in group 1 (control) and group 2 (l-carnitine) were injected intraperitoneal (i.p.) with normal saline and l-carnitine (200 mg/kg/day), respectively, for 10 successive days. Animals in group 3 (CP group) were injected i.p. with normal saline for 5 days before and 5 days after a single dose of CP (200 mg/kg, i.p.). Rats in group 4 (IFO group) received normal saline for 5 successive days followed by IFO (50 mg/kg/day, i.p.) for 5 successive days. Rats in group 5 (CP-carnitine supplemented) were given the same doses of l-carnitine as group 2 for 5 days before and 5 days after a single dose of CP as group 3. Rats in group 6 (IFO-carnitine supplemented) were given the same doses of l-carnitine as group 2 for 5 days before and 5 days concomitant with IFO as group 4. Immediately, after the last dose of the treatment protocol, blood samples were withdrawn and animals were killed for biochemical, histopathological and gene expression studies. Treatment with CP and IFO significantly decreased expression of heart fatty acid binding protein (H-FABP) and carnitine palmitoyltransferase I (CPT I) genes in cardiac tissues. Moreover, CP but not IFO significantly increased acetyl-CoA carboxylase2 mRNA expression. Conversely, IFO but not CP significantly decreased mRNA expression of malonyl-CoA decarboxylase. Both CP and IFO significantly increased serum lactate dehydrogenase, creatine kinase isoenzyme MB and malonyl-CoA content and histopathological lesions in cardiac tissues. Interestingly, carnitine supplementation completely reversed all the biochemical, histopathological and gene expression changes induced by CP and IFO to the control values, except CPT I mRNA, and protein expression remained inhibited by IFO. Data from the current study suggest, for the first time, that (1) CP and IFO therapy is associated with the inhibition of the expression of H-FABP and CPT I genes in cardiac tissues with the consequent inhibition of mitochondrial transport and oxidation of LCFA. (2) The progressive increase in cardiotoxicity enzymatic indices and the decrease in H-FABP and CPT I expression may point to the possible contribution of these genes to CP- and IFO-induced cardiotoxicity.     

Protective effect of arabic gum against acetaminophen-induced hepatotoxicity in mice

Overdose of acetaminophen, a widely used analgesic drug, can result in severe hepatotoxicity and is often fatal. This study was undertaken to examine the effects of arabic gum (AG), which is commonly used in processed foods, on acetaminophen-induced hepatotoxicity in mice. Mice were given arabic gum orally (100 g l(-1)) 5 days before a hepatotoxic dose of acetaminophen (500 mg kg(-1)) intraperitoneally. Arabic gum administration dramatically reduced acetaminophen-induced hepatotoxicity as evidenced by reduced serum alanine (ALT) and aspartate aminotransferase (AST) activities. Acetaminophen-induced hepatic lipid peroxidation was reduced significantly by arabic gum pretreatment. The protection offered by arabic gum does not appear to be caused by a decrease in the formation of toxic acetaminophen metabolites, which consumes glutathione, because arabic gum did not alter acetaminophen-induced hepatic glutathione depletion. Acetaminophen increased nitric oxide synthesis as measured by serum nitrate plus nitrite at 4 and 6 h after administration and arabic gum pretreatment significantly reduced their formation. In conclusion, arabic gum is effective in protecting mice against acetaminophen-induced hepatotoxicity. This protection may involve the reduction of oxidative stress.     

Psychiatrische Notfälle in der pädiatrischen Ambulanz

Mental disorders are common phenomena in childhood and adolescence and patients with psychiatric symptoms are frequently referred to emergency pediatric departments depending on local healthcare conventions. This article provides recommendations for this treatment situation on the basis of the available scientific evidence.     

Spontaneous heterotopic pregnancy presenting with tubal rupture

We present the case of a woman who sought pregnancy termination but who, in the interval between consultation and surgical termination, presented with clinical signs of a ruptured ectopic pregnancy. This was managed as such, but post-operative follow-up soon revealed that she also carried a viable intrauterine pregnancy.      

Elevated mitochondrial cisplatin-DNA adduct levels in rat tissues after transplacental cisplatin exposure

Although there is evidence that the toxic effects of cis- diamminedichloroplatinum(II) (cisplatin) include morphologically abnormal mitochondria, direct demonstrations of mitochondrial DNA damage by this chemotherapeutic agent have rarely been reported. Here we show that, in rats exposed to a single dose of cisplatin during gestation, cisplatin-DNA binding levels in both maternal and fetal liver and brain mitochondrial DNA are higher than those observed in genomic DNA. Pregnant F344/NCr rats were injected i.p. with either 5 or 15 mg cisplatin/kg body wt at 18 days of gestation and killed 24 h later. Cisplatin-DNA adducts were determined by dissociation-enhanced lanthanide fluoroimmunoassay using a cisplatin-DNA standard modified in the same range as the biological samples. Values for genomic cisplatin- DNA adducts in multiple maternal and fetal tissues have been presented elsewhere. Here, genomic DNA adduct levels for liver, brain, kidney and placenta are reported again for comparison with mitochondrial DNA adduct levels in the same tissues. In maternal and fetal brain, mitochondrial DNA adduct levels were approximately 7- to 50-fold higher than genomic DNA adduct levels, and in fetal liver they were approximately 2- to 16-fold higher than genomic DNA adduct levels. These studies demonstrate extensive cisplatin-DNA adduct formation in brain and liver mitochondria of fetal rats exposed transplacentally and suggest that mitochondrial DNA in some organs may be a particular target for cisplatin genotoxicity.