Staphylococcus aureus meningitis: experience with cefuroxime treatment during a 16 year period in a Danish region

Staphylococcus aureus is a rare cause of bacterial meningitis and there is no consensus on antibiotic treatment. Nafcillin is a common choice in countries where it is approved and marketed. High-dose cefuroxime has been the systemic treatment used in the study region, and a retrospective record review was conducted to determine its clinical efficacy. Cases of bacterial meningitis during 1984-1999 in the County of North Jutland, Denmark (approx. 490000 inhabitants), were identified in a regional bacteriology register. Inclusion of a case required either growth of S. aureus from > or = 2 specimens of cerebrospinal fluid (CSF), 1 positive CSF specimen with a CSF leucocyte count > 10(8)/l or 1 positive CSF specimen with a concurrent positive blood culture. A diagnosis of brain abscess required growth of S. aureus from aspirated pus. Staphylococcus aureus meningitis was confirmed in 45 patients, and 5 additional patients had a brain abscess. 44 cases were nosocomial (mortality 16%) and 6 were community acquired (mortality 83%). None of the isolates was methicillin resistant and 6 were penicillin susceptible. Intraventricular antibiotic treatment was given to 28 patients, systemic therapy included cefuroxime in 32 patients (64%) as either a primary or secondary choice, 6 (12%) were treated with penicillin G, 10 (20%) with penicillinase-resistant penicillin and 2 (4%) with cephalothin. Among 31 nosocomial cases treated systemically with cefuroxime the mortality was 10% (95% exact confidence limits 2-26%). In conclusion, cefuroxime seems to be a valid choice for S. aureus meningitis in the nosocomial setting.     

Aortocaval fistula after stent-graft repair.

PURPOSE: To report an aortocaval fistula after stent-graft repair and the feasibility of interventional treatment. CASE REPORT: A 78-year-old man with a 61-mm infrarenal aortic aneurysm (AA) was treated successfully with a Zenith bifurcated stent-graft. Three years later, the patient presented with deteriorating renal function and acute bronchial obstruction. Computed tomography showed an aortic diameter increased to 90 mm, dilatation of the inferior vena cava, and a distal type I endoleak. The patient's condition quickly deteriorated, and emergent imaging found a fistula with brisk flow between the aneurysm sac and the left iliac vein within a distal type I endoleak. During emergency endovascular repair, iliac extensions were implanted in the right common iliac artery and left external iliac artery. The left hypogastric artery was coil embolized to exclude flow into the aneurysm sac. After positioning the extensions, cardiac function improved, and the fistula was no longer palpable. The cardiac indices and renal function normalized, and he was discharged 20 days after admission. CONCLUSION: Aortocaval fistulas are a rare complication of AA stent-graft repair and may be successfully treated by interventional means.     

Pancreatic exocrine insufficiency in LXRbeta-/- mice is associated with a reduction in aquaporin-1 expression

Liver X receptors (LXRs) α and β are nuclear oxysterol receptors with a key role in cholesterol, triglyceride, and glucose metabolism. In LXRβ^−/− mice on a normal diet, there is a reduction in size of perigonadal fat pad and, on high-fat diet there is resistance to obesity. In the present study, we investigated the reason for the resistance of LXRβ^−/− mice to weight gain. In LXRβ^−/− mice we found pancreatic exocrine insufficiency with reduced serum levels of amylase and lipase, reduced proteolytic activity in feces, chronic inflammatory infiltration, and, in the ductal epithelium, an increased apoptosis without compensatory proliferation. Electron microscopy revealed ductal dilatation with intraductal laminar structures characteristic of cystic fibrosis. To investigate the relationship between LXRβ and pancreatic secretion, we studied the expression of LXRβ and the water channel, aquaporin-1 (AQP1), in the ductal epithelium of the pancreas. In WT mice, ductal epithelial cells expressed LXRβ in the nuclei and AQP1 on the plasma membrane. In LXRβ^−/− mice neither LXRβ nor AQP1 was detectable. Moreover, in WT mice the LXR agonist (T2320) increased AQP1 gene expression. These data demonstrate that in LXRβ^−/− mice dietary resistance to weight gain is caused by pancreatic insufficiency and that LXRβ regulates pancreatic exocrine secretion through the control of AQP1 expression. Pancreatic exocrine insufficiency is the main cause of malabsorption syndrome responsible for weight loss in adults and growth failure in children. Several genes are known to be involved in the pathogenesis and susceptibility to pancreatic insufficiency. LXRβ should be included in that list.     

Outcome‐dependent coactivation of lip and tongue primary somatosensory representation following hypoglossal–facial transfer after peripheral facial palsy

A hypoglossal–facial transfer is a common surgical strategy for reanimating the face after persistent total hemifacial palsy. We were interested in how motor recovery is associated with cortical reorganization of lip and tongue representation in the primary sensorimotor cortex after the transfer. Therefore, we used functional magnetic resonance imaging (fMRI) in 13 patients who underwent a hypoglossal–facial transfer after unilateral peripheral facial palsy. To identify primary motor and somatosensory tongue and lip representation sites, we measured repetitive tongue and lip movements during fMRI. Electromyography (EMG) of the perioral muscles during tongue and lip movements and standardized evaluation of lip elevation served as outcome parameters. We found an association of cortical representation sites in the pre‐ and postcentral gyrus (decreased distance of lip and tongue representation) with symmetry of recovered lip movements (lip elevation) and coactivation of the lip during voluntary tongue movements (EMG‐activity of the lip during tongue movements). Overall, our study shows that hypoglossal–facial transfer resulted in an outcome‐dependent cortical reorganization with activation of the cortical tongue area for restituded movement of the lip. Hum Brain Mapp 35:638–645, 2014. © 2012 Wiley‐Periodicals, Inc.     

The Contribution of the Left Phrenic Nerve to Innervation of the Esophagogastric Junction

The contribution of the left phrenic nerve to innervation of the esophagogastric junction. The esophagogastric junction is part of the barrier preventing gastroesophageal reflux. We have investigated the contribution of the phrenic nerves to innervation of the esophagogastric junction in humans and piglets by dissecting 30 embalmed human specimens and 14 piglets. Samples were microdissected and nerves were stained and examined by light and electron microscopy. In 76.6% of the human specimens, the left phrenic nerve participated in the innervation of the esophagogastric junction by forming a neural network together with the celiac plexus (46.6%) or by sending off a distinct phrenic branch, which joined the anterior vagal trunk (20%). Distinct left phrenic branches were always accompanied by small branches of the left inferior phrenic artery. In 10% there were indirect connections with a distinct phrenic nerve branch joining the celiac ganglion, from which celiac plexus branches to the esophagogastric junction emerged. Morphological examination of phrenic branches revealed strong similarities to autonomic celiac plexus branches. There was no contribution of the left phrenic nerve or accompanying arteries from the caudal phrenic artery in any of the piglets. The right phrenic nerve made no contribution in any of the human or piglet samples. We conclude that the left phrenic nerve in humans contributes to the innervation of the esophagogastric junction by providing ancillary autonomic nerve fibers. Experimental studies of the innervation in pigs should consider that neither of the phrenic nerves was found to contribute. Clin. Anat. 33:265–274, 2020. © 2019 Wiley Periodicals, Inc.