Aortopexy for tracheomalacia via a suprasternal incision

Aim

Tracheomalacia is flaccidity of the tracheal wall leading to tracheal collapse, particularly on expiration. When severe it can warrant surgical intervention. Aortopexy is one surgical option and has been described using a variety of approaches. We report outcomes of aortopexy performed via a suprasternal incision in a single centre by a single surgeon.

Does Meningitis Stop CSF Rhinorrhea following Lateral Skull Base Surgery?

In cases of cerebrospinal fluid (CSF) rhinorrhea following lateral skull base surgery, fibrosis and fibrin formation resulting from meningitis has been postulated as a mechanism of spontaneously resolving the CSF leak. This study was undertaken to explore any possible relationship between the cessation of CSF leak and meningitis. A retrospective study at a tertiary referral center of 232 consecutive patients was performed. Out of a total of 232 procedures, 29 patients developed CSF rhinorrhea, of whom 7 subsequently developed meningitis. Bacteria were isolated in CSF obtained at lumbar puncture in 5 cases, with the CSF analysis in the remaining 2 cases suggesting aseptic meningitis. Conservative treatment failed to stop the CSF rhinorrhea in 6 of 7 cases. In this study, the development of meningitis did not appear to aid in the resolution of the CSF rhinorrhea. We conclude that surgical intervention should not be delayed in the expectation that meningitis and conservative interventions may promote CSF leak resolution.     

Prediction and prevention of anastomotic complications of esophageal atresia and tracheoesophageal fistula

We analyzed our experience with 64 infants with esophageal atresia (EA) and tracheoesophageal fistula (TEF), to determine the possibility of prediction and prevention of anastomotic complications (leak, stricture, and recurrent TEF). In most of the infants, the anatomical level of the fistula was documented preoperatively by bronchoscopy. The level of the fistula, in turn, correlated with the esophageal anatomy at thoracotomy, ie, carinal fistulas had a wide gap between esophageal pouches, whereas midtracheal or cervical fistulas had a minimal gap. Major anastomotic complications were defined as leak requiring reoperation, symptomatic strictures requiring four or more dilatations, or a recurrent TEF. The complication rates wre: leak (major and minor), 21%; major stricture, 15%; and recurrent TEF, 5%. Major complications occurred in 42% (11/26) of infants with wide gaps, compared with 8% (3/36) of infants with minimal gaps. Route of repair (transpleural or retropleural) made no difference in incidence of anastomotic complications. No infant died of an anastomotic complication. Survival was 100% for Waterston A and B infants, 83% for Waterston C, and 90% overall. Severe gastroesophageal reflux, requiring Nissen fundoplication, was more common among infants with wide gaps than those with minimal gaps (32% v 3%). The most important pathogenetic factor, present in 79% (11/14) of major anastomotic complications, was anastomotic tension, determined by the gap between esophageal pouches, and predicted by preoperative bronchoscopy. Thus the bronchoscopic finding of a carinal fistula signals the need for technical measures that may limit anastomotic morbidity, such as myotomy, patching the anastomosis, retropleural approach, or delayed repair. Assuming precise technique and gentle handling of tissues, the anatomy of the anomaly determines the anastomotic morbidity of EA and TEF.     

PLASMA FOLLISTATIN CONCENTRATIONS INCREASE FOLLOWING LIPOPOLYSACCHARIDE ADMINISTRATION IN SHEEP

1. The effect of inflammation induced by lipopolysaccharide (LPS) injection on plasma follistatin (FS) concentrations was investigated. 2. Plasma FS and tumour necrosis factor-α concentrations increase following LPS administration in ewes. 3. The rise in FS is similar, but more sustained, to that previously observed after surgery. 4. These results indicate a possible functional link between FS, inflammation and the acute-phase response.     

Smaller hippocampal volume in patients with recent-onset posttraumatic stress disorder.

BACKGROUND: Previous structural magnetic resonance (MR) research in patients with posttraumatic stress disorder (PTSD) has found smaller hippocampal volumes in patients compared with control subjects. These studies have mostly involved subjects who have had PTSD for a number of years, such as war veterans or adult survivors of childhood abuse. Patients with recent-onset PTSD have rarely been investigated. To our knowledge only one other study has investigated such a group. The aim of this study was to compare hippocampal volumes of patients with recent onset PTSD and nontrauma-exposed control subjects. METHODS: Fifteen patients with PTSD, recruited from an accident and emergency department, were compared with 11, non-trauma-exposed, healthy control subjects. Patients underwent a structural MR scan soon after trauma (mean time = 158 +/- 41 days). Entire brain volumes, voxel size 1 x 1 x 1 mm, were acquired for each subject. Point counting and stereology were used to measure the hippocampal and amygdala volume of each subject. RESULTS: Right-sided hippocampal volume was significantly smaller in PTSD patients than control subjects after controlling for effects of whole brain volume and age. Neither left nor total hippocampal volume were significantly smaller in the PTSD group after correction. Whole brain volume was also found to be significantly smaller in patients. There were no differences in amygdala or white matter volumes between patients and control subjects. CONCLUSIONS: This result replicates previous findings of smaller hippocampal volumes in PTSD patients, but in an underinvestigated population, suggesting that either smaller hippocampal volume is a predisposing factor in the development of PTSD or that damage occurs within months of trauma, rather than a number of years. Either of these two hypotheses have significant implications for the treatment of PTSD. For instance, if it could be shown that screening for hippocampal volume may, in some cases, predict those likely to develop clinical PTSD.     

Exacerbation of lymphocytic choriomeningitis in mice treated with the inducible nitric oxide synthase inhibitor aminoguanidine

To elucidate the possible involvement of the inducible nitric oxide synthase (iNOS) and NO in the development of lymphocytic choriomeningitis (LCM), the consequences of inhibition of iNOS by the inhibitor aminoguanidine was examined in mice following intracerebral infection with LCM virus (LCMV). Aminoguanidine administration to mice infected with LCMV completely blocked increased plasma nitrate/nitrite levels and led to increased proinflammatory cytokine gene expression at early stages of lesion development in the brain, enhanced clinical severity and decreased survival time. The levels of LCMV recovered from the brain of aminoguanidine treated mice did not differ from those in infected control mice. These findings argue against either an anti-viral or pathogenic role of NO in LCM but rather suggest a possible protective action of this mediator.