Technik des Sternumverschlusses

Median sternotomy remains the most common surgical incision used by cardiothoracic surgeons. The purpose of this paper is to summarize the pros and cons of the different sternal closure techniques and their principles by concentrating on their clinical and biomechanical aspects. Unfortunately, there are no adequately powered, prospective randomized controlled clinical trials comparing different osteosynthetic techniques with regard to sternal instability. Therefore, the level of evidence is rather weak. Furthermore, there is no consensus among biomechanical studies on the optimal sternal model and the effectiveness of different methods for sternal closure. Key factors in preventing sternal dehiscence are compliance with rules of aseptic surgery and osteosynthesis, suture of rectus fascia respecting anatomic compartments, additional reinforcement of the lower third of the sternum and careful attention to hemostasis.     

Sternal closure techniques and postoperative sternal wound complications in elderly patients.

OBJECTIVE: Postoperative sternal wound complications (PSWC) including deep sternal wound infection (DSWI) and sternal dehiscence (SD) cause significant morbidity and mortality. Elderly patients with several risk factors are particularly prone to suffer PSWC. METHODS: We present (I) a subset of 86 patients, all aged > or =75 years out of 339 cardiac surgery patients prospectively randomised to receive either conventional sternal closure or a Robicsek type closure. Primary end-points were SD and DSWI; secondary end-points included a composite of clinical parameters; (II) we retrospectively assessed data of 54/5273 patients with mediastinitis regarding the influence of advanced age. In addition, we report an epidemiological overview of different sternal closure techniques. RESULTS: (I) The Robicsek technique showed an impact on SD and DSWI, and several secondary end-points: ventilator support (p=0.03), postoperative blood loss (p=0.04), and chest pain >3 days (p=0.04). (II) A total of 54/5273 (1.02%) patients developed postoperative mediastinitis. Twelve out of 54 (22%) patients died within 6 months of the initial operation. Predictors of mortality were insulin-dependent diabetes mellitus (p=0.05), renal insufficiency (p=0.01), delayed sternal closure (p=0.05), ICU-stay >10 days (p=0.01), and methicillin-resistant Staphylococcus aureus (p=0.03) or fungal infection (p=0.02). CONCLUSIONS: No statistical difference in sternal dehiscence or mediastinitis was found irrespective of whether the bilateral and longitudinal parasternal closure or the conventional peri/trans-sternal wiring technique was used, but there was an obvious, positive influence on sternal dehiscence, deep sternal wound infection, and clinical parameters. However, the study population is relatively small.     

Oxygen toxicity in the newborn lung: reversal of inhibition of DNA synthesis in the mouse.

Continuous exposure to 100% oxygen at atmospheric pressure for two weeks causes significant alterations in the growth of the lung and the body of newborn mice. These changes can be divided into three phases. The initial phase, which lasts 96 hours, is characterized by inhibition of lung DNA synthesis, diminished total lung DNA, and a decrease in the ratio of lung DNA to body weight. The intermediate phase from 96 to 144 hours is characterized by a sharp increase in mortality, a plateau in body weight, and a minimal lung DNA/body weight ratio. During this period, however, surviving animals show a reversal of the inhibition of DNA synthesis and thus an increase in total lung DNA. The third phase, occurring after 144 hours, is characterized by a continued increase in DNA synthesis and total lung DNA, a gain in body weight, a return of the lung DNA/body weight ratio to control levels, and a sharp decline in mortality. The survival rate of 54% in newborn mice over two weeks contrasts with the near total mortality reported for adult experimental animals similarly exposed. The reversal of the inhibition of lung DNA synthesis in surviving mice suggests either that some newborn animals are inherently resistant to pulmonary oxygen toxicity or that they develop, during a critical exposure period, an adaptive process necessary for their survival.     

Minisatellite rearrangements are increased in liver tumours induced by transplacental aflatoxin B1 treatment of hepatitis B virus transgenic mice, but not in spontaneously arising tumours

Transgenic mice carrying an integrated subgenomic human hepatitis B virus (HBV) DNA fragment coding for the viral envelope polypeptides, represent a model for the study of the mechanisms involved in hepatocarcinogenesis. The mice develop a progressive liver injury characterized by inflammation, regenerative hyperplasia and dysplasia terminating in hepatocellular carcinoma (HCC) at around 18-21 months of age. No alterations in specific oncogenes and tumour suppressor genes in the HCC arising in this transgenic model have been observed. However, onset of liver tumours is significantly earlier in mice treated with aflatoxin B1 (AFB1). In order to examine more generally for genetic rearrangements during the natural history of the disease, DNA multilocus fingerprinting was performed using probes recognizing mouse minisatellites. Liver tumour samples from HBV transgenic mice either untreated or treated with AFB1 transplacentally were included in the study. In a total of 28 tumour samples from HBV transgenic mice receiving no carcinogen treatment, using three minisatellite probes, no alterations were detected. The frequency of rearrangements using any one of the three probes is calculated to be below 0.2%. This result demonstrates that genetic instability in minisatellite sequences is not a common event associated with HBV gene expression and liver injury in this model. In 11 liver tumours from mice exposed to AFB1 transplacentally six had minisatellite alterations (band gains and losses) revealed by at least one of the three probes used. The frequency of rearrangements was between 1.1% and 2% depending on the minisatellite probe. These data show that genetic alterations can be induced by transplacental exposure to AFB1 and suggest that genetic instability could be important in hepatocarcinogenesis with combined exposures to AFB1 and HBV.      

Emotional and attentive interferences and slow cerebral potentials (CNV-P 300) (author's transl)

A study was conducted to establish possible correlations between electrophysiological indices and performance under neutral situations and those involving completing a double task of increasing complexity, by studying CNV and P 300 in young healthy men. The results demonstrated that: 1. After habituation, the CNV amplitudes were not related to performance. A significant correlation was noted only during the most complex tasks. 2. The CNV appears to depend mainly on endogenous factors, that is to say the aptitude and readiness of an individual to treat the information, rather than on the performance resulting from this treatment. 3. The amplitude of the P 300 is related to performance, as a function of detection rate and the complexity of the tasks. The functional duality of the CNV and the differences between it and the P 300 have been emphasized. The indices obtained from slow potentials appear to be of value for an evaluation of behaviour. Rather than analyzing the characteristics of the potentials in a supposedly "neutral" situation it would appear preferable to establish, from the indices, profiles of individual reactivity and adaptation to different experimental situations.     

Inhaled mometasone furoate reduces oral prednisone requirements while improving respiratory function and health-related quality of life in patients with severe persistent asthma

BACKGROUND: Inhaled corticosteroid therapy in severe persistent asthma has been shown to reduce or eliminate oral corticosteroid (OCS) use while retaining effective asthma control. OBJECTIVE: We sought to evaluate the ability of mometasone furoate (MF) delivered by means of dry powder inhaler to reduce daily oral prednisone requirements in OCS-dependent patients with severe persistent asthma. METHODS: We performed a 12-week, double-blind, placebocontrolled trial (21 centers, 132 patients) comparing 2 doses of MF (400 and 800 microg administered twice daily) with placebo, followed by a 9-month open-label phase in which 128 patients received treatment with MF. RESULTS: At the endpoint of the double-blind trial, MF 400 and 800 mg twice daily reduced daily OCS requirements by 46.0% and 23.9%, respectively, whereas placebo increased OCS requirements by 164.4% (P <.01). Oral steroids were eliminated in 40%, 37%, and 0% of patients in the MF 400 and 800 mg twice daily and placebo groups, respectively. Pulmonary function and quality of life significantly increased for MF-treated patients. Further reductions in OCS requirements were achieved with long-term MF treatment in the open-label phase. CONCLUSION: MF inhaled orally as a dry powder is an effective alternative to systemic corticosteroids in patients with severe persistent asthma.     

Evaluation of cytokines in nasal secretions after nasal antigen challenge: lack of influence of antihistamines.

BACKGROUND: Previous studies of inflammation in allergic rhinitis using nasal irrication have been unsatisfactory because of 1) poor reproducibility; 2) the tendency of irrigation to overdilute mediators; and 3) the failure of this technique to evaluate interstitial concentrations of relevant mediators. For this study we used filter paper as a matrix to collect nasal secretions in patients undergoing nasal antigen challenge. OBJECTIVE: To evaluate inflammatory mediators of allergen-induced rhinitis during a clinical trial of fexofenadine. METHODS: Subjects evaluated at a referral medical center were placed on traditional dosing of fexofenadine at 60 mg, twice daily, or placebo in a double-blind, crossover fashion for 1 week before the nasal challenge. Nasal challenge was performed with nasal insufflation of either 1,000 AU timothy or 0.1 mL ragweed (1:100 wt/vol) extract outside the pollen season. Nasal secretions were collected at baseline and then at 2, 4, and 6 hours after nasal challenge. Secretions were evaluated for expression of the cellular adhesion molecule-1, tumor necrosis factor (TNF)-alpha, interleukin (IL)-4, IL-10, macrophage inflammatory protein (MIP)-1alpha, and granulocyte-macrophage colony-stimulating factor (GM-CSF) using commercially available enzyme-linked immunoadsorbent assay kits. Patients' symptom scores were evaluated during the nasal challenge. RESULTS: Significantly (P < 0.05) increased peak levels of TNF-alpha, IL-4, IL-10, and MIP-1alpha were detected after antigen challenge as compared with baseline levels. There was a nonsignificant trend toward an increase in GM-CSF after antigen challenge (P = 0.07). There was no difference in the peak levels of TNF-alpha, IL-4, IL-10, MIP-1alpha, or GM-CSF measured when patients were on fexofenadine versus placebo. Finally, there were no significant differences in patients' symptom scores during antigen challenge when subjects were on fexofenadine versus placebo. CONCLUSIONS: Collection of nasal secretions using a filter paper matrix provides a reproducible model for accurately detecting and evaluating changes in cytokine levels after nasal challenge. Cytokine levels tend to peak 3 to 4 hours after antigen challenge. Standard doses of fexofenadine do not seem to have a mitigating effect on the production of these cytokines. Symptoms of allergic rhinitis using this type of antigen challenge did not differ from treatment with fexofenadine versus placebo.     

The normal human thymic vasculature: an ultrastructural study.

Electron microscopy of the normal human thymus demonstrates a characteristic vascular-parenchymal relationship. The vascular lumen is always separated from the thymic parenchyma by: the endothelial cell cytoplasm, a muscular coat in arterioles and veins, the vascular basal lamina, a perivascular space containing collagen fibers and cells, the epithelial-reticular cell basal lamina and the epithelial-reticular cell cytoplasm. The width of this perivascular space is proportional to the size of the vessel it surrounds; it is wide around the vessels in the septa and at the cortical-medullary junction, but narrow around capillaries. While many cells are present in this space around larger vessels, only collagen is observed around the capillaries. Lymphocytes are the predominant cell type in the space; however, plasma cells, eosinophils, histiocytes, polymorphonuclear leukocytes, mast cells and unidentified granulated cells are also seen. The vascular complex described above may function as a blood-thymus barrier, as the initial site of exposure of the lymphocytes to circulating antigen and as the route of lymphocytes from the thymus.     

On the origin of the membranous intraalveolar material in pulmonary alveolar proteinosis

A case of pulmonary alveolar proteinosis, studied by light and electron microscopy, showed evidence for increased secretion of lamellar bodies by granular pneumocytes, uptake of these lamellar bodies by alveolar macrophages and eventual disintegration of the macrophages. These findings are assumed to be the main events in the pathogenesis of this disease. The same sequence leading to a condition morphologically resembling alveolar proteinosis can be found in an experimental model using prolonged exposure of newborn mice to 100% oxygen. In both instances, the membranous component of the proteinaceous material (myeloid bodies) appeared to originate from the ingested lamellar bodies in lysosomes of alveolar macrophages. It is suggested that this conversion of lamellar bodies is a physiologic mode of inactivation of surfactant, and that pulmonary alveolar proteinosis represents a state in which the catabolic capacities of alveolar macrophages have been overstressed.