Infection prevention during anaesthesia ventilation by the use of breathing system filters (BSF): Joint recommendation by German Society of Hospital Hygiene (DGKH) and German Society for Anaesthesiology and Intensive Care (DGAI)

An interdisciplinary working group from the German Society of Hospital Hygiene (DGKH) and the German Society for Anaesthesiology and Intensive Care (DGAI) worked out the following recommendations for infection prevention during anaesthesia by using breathing system filters (BSF). The BSF shall be changed after each patient. The filter retention efficiency for airborne particles is recommended to be >99% (II). The retention performance of BSF for liquids is recommended to be at pressures of at least 60 hPa (=60 mbar) or 20 hPa above the selected maximum ventilation pressure in the anaesthetic system

Cost analysis of two anaesthetic machines: "Primus^®" and "Zeus^®"

Abstract Background Two anaesthetic machines, the "Primus®" and the "Zeus®" (Draeger AG, Lübeck, Germany), were subjected to a cost analysis by evaluating the various expenses that go into using each machine. Methods These expenses included the acquisition, maintenance, training and device-specific accessory costs. In addition, oxygen, medical air and volatile anaesthetic consumption were determined for each machine. Results Anaesthesia duration was 278 ± 140 and 208 ± 112 minutes in the Primus® and the Zeus®, respectively. The purchase cost was €3.28 and €4.58 per hour of operation in the Primus® and the Zeus®, respectively. The maintenance cost was €0.90 and €1.20 per hour of operation in the Primus® and the Zeus®, respectively. We found that the O2 cost was €0.015 ± 0.013 and €0.056 ± 0.121 per hour of operation in the Primus® and the Zeus®, respectively. The medical air cost was €0.005 ± 0.003 and €0.016 ± 0.027 per hour of operation in the Primus® and the Zeus®, respectively. The volatile anaesthetic cost was €2.40 ± 2.40 and €4.80 ± 4.80 per hour of operation in the Primus® and the Zeus®, respectively. Conclusion This study showed that the "Zeus®" generates a higher cost per hour of operation compared to the "Primus®".</p

Ex vivo water exchange performance and short-term clinical feasibility assessment of newly developed heat and moisture exchangers for pulmonary rehabilitation after total laryngectomy

Laryngectomized patients suffer from respiratory complaints due to insufficient warming and humidification of inspired air in the upper respiratory tract. Improvement of pulmonary humidification with significant reduction of pulmonary complaints is achieved by the application of a heat and moisture exchanger (HME) over the tracheostoma. The aim of this study was to determine whether the new Provox HMEs (XM-HME and XF-HME) have a better water exchange performance than their predecessors (R-HME and L-HME, respectively; Atos Medical, Hörby, Sweden). The other aim was to assess the short-term clinical feasibility of these HMEs. The XM-HME and XF-HME were weighed at the end of inspiration and at the end of expiration at different breathing volumes produced by a healthy volunteer. The associations between weight changes, breathing volume and absolute humidity were determined using both linear and non-linear mixed effects models. Study-specific questionnaires and tally sheets were used in the clinical feasibility study. The weight change of the XM-HME is 3.6 mg, this is significantly higher than that of the R-HME (2.0 mg). The weight change of the XF-HME (2.0 mg) was not significantly higher than that of the L-HME (1.8 mg). The absolute humidity values of both XM- and XF-HME were significantly higher than that of their predecessors. The clinical feasibility study did not reveal any practical problems over the course of 3 weeks. The XM-HME has a significantly better water exchange performance than its predecessor (R-HME). Both newly designed HMEs did succeed in the clinical feasibility stud

Mitochondrial deficits and abnormal mitochondrial retrograde axonal transport play a role in the pathogenesis of mutant Hsp27-induced Charcot Marie Tooth Disease

Mutations in the small heat shock protein Hsp27, encoded by the HSPB1 gene, have been shown to cause Charcot Marie Tooth Disease type 2 (CMT-2) or distal hereditary motor neuropathy (dHMN). Protein aggregation and axonal transport deficits have been implicated in the disease. In this study, we conducted analysis of bidirectional movements of mitochondria in primary motor neuron axons expressing wild type and mutant Hsp27. We found significantly slower retrograde transport of mitochondria in Ser135Phe, Pro39Leu and Arg140Gly mutant Hsp27 expressing motor neurons than in wild type Hsp27 neurons, although anterograde movement velocities remained normal. Retrograde transport of other important cargoes, such as the p75 neurotrophic factor receptor was minimally altered in mutant Hsp27 neurons, implicating that axonal transport deficits primarily affect mitochondria and the axonal transport machinery itself is less affected. Investigation of mitochondrial function revealed a decrease in mitochondrial membrane potential in mutant Hsp27 expressing motor axons, as well as a reduction in mitochondrial complex 1 activity, increased vulnerability of mitochondria to mitochondrial stressors, leading to elevated superoxide release and reduced mitochondrial glutathione (GSH) levels, although cytosolic GSH remained normal. This mitochondrial redox imbalance in mutant Hsp27 motor neurons is likely to cause low level of oxidative stress, which in turn will contribute to, and indeed may be the underlying cause of the deficits in mitochondrial axonal transport. Together, these findings suggest that mitochondrial abnormalities in mutant Hsp27-induced neuropathies may be a primary cause of pathology, leading to further deficits in mitochondrial axonal transport and onset of disease

Mutations in a Gene Encoding a Novel SH3/TPR Domain Protein Cause Autosomal Recessive Charcot-Marie-Tooth Type 4C Neuropathy

Charcot-Marie-Tooth disease type 4C (CMT4C) is a childhood-onset demyelinating form of hereditary motor and sensory neuropathy associated with an early-onset scoliosis and a distinct Schwann cell pathology. CMT4C is inherited as an autosomal recessive trait and has been mapped to a 13-cM linkage interval on chromosome 5q23-q33. By homozygosity mapping and allele-sharing analysis, we refined the CMT4C locus to a suggestive critical region of 1.7 Mb. We subsequently identified mutations in an uncharacterized transcript, KIAA1985, in 12 families with autosomal recessive neuropathy. We observed eight distinct protein-truncating mutations and three nonconservative missense mutations affecting amino acids conserved through evolution. In all families, we identified a mutation on each disease allele, either in the homozygous or in the compound heterozygous state. The CMT4C gene is strongly expressed in neural tissues, including peripheral nerve tissue. The translated protein defines a new protein family of unknown function with putative orthologues in vertebrates. Comparative sequence alignments indicate that members of this protein family contain multiple SH3 and TPR domains that are likely involved in the formation of protein complexes