Citations

Introduction: Abdominal aortic aneurysm (AAA) rupture has a mortality rate of 64% and intracranial aneurysm (IA) rupture has a mortality rate of 50%. Despite the high mortality rates, early detection and treatment of these vascular lesions prior to rupture can prevent devastating clinical outcomes, underscoring the need to identify high-risk populations for screening. Current evidence demonstrates shared genetic and environmental risk factors for both AAA and IA. Methods: The BAAS study sought to establish the co-prevalence of AAA and IA. In one arm of BAAS, we recruited patients presenting with AAA and screened them for IA. All participants underwent a detailed interview to collect demographic, radiographic, and clinical data and also had genetic counseling. Results: Of the 126 individuals with an AAA enrolled, 65% (82/126) completed the MRA. Difficulty with logistics of obtaining the research MRA with long distance travel to clinic was the principal reason for failure to obtain MRA. We identified 20.7% (17/82) with one or more IA, including 21 aneurysms found during systematic screening. IA ranged in size from 1.5-14 mm (height) x 1.4-7 mm (width) and varied in location. 9.5% (2/21) had a maximum diameter of 7 mm or more. One participant with a positive MRA underwent early coil embolization with the remainder undergoing continued clinical surveillance. Of the 15 individuals completing the genetic counseling screening, two underwent recommended clinical genetic testing, revealing one negative screen and one variant of unknown significance in the MYH11 gene. Conclusion: Consistent with our prior cost effectiveness models, these prospective data support the clinical utility of routine screening for IA in patients presenting with AAA.

Objectives: To validate a neck-shaft angle (NSA) correction formula using the known angle between the medullary nail and lag screw of an indwelling cephalomedullary nail (CMN). Methods: Pertrochanteric femur fractures were created in 7 synthetic femurs and reconstructed with a CMN. Anteroposterior x-rays were taken with the proximal femur in 0, 15, 30, and 45 degrees of internal/external rotation and 10 and 20 degrees of flexion with neutral rotation. The femoral NSA and the nail angle were measured on anteroposterior x-rays. The corrected NSA was obtained by multiplying the known nail angle by the quotient of the measured NSA over the measured nail angle. Results: With increasing degrees of internal or external rotation, the difference between the actual and the measured NSA increased. After correction using the known angle of the nail, the measured NSA was reduced to within 3 degrees of the actual NSA over all degrees of rotation. At neutral rotation, 15 degrees of external rotation, and 10 and 20 degrees of hip flexion, there was minimal difference between the actual NSA and the measured NSA, negating the effect of the correction formula. Conclusions: The measured NSA after CMN of intertrochanteric fractures is altered by hip rotation. This study validates the correction formula, which determines this difference by using the known angle between the lag screw and the nail.

Abstract Background The neo-squamous epithelium that replaces columnar epithelium after successful endoscopic ablation of Barrett's esophagus (BE) has not been fully characterized in regard to its structural and functional integrity. Intercellular space is a surrogate marker for epithelial structural integrity and mucosal impedance (MI) is a surrogate for transepithelial resistance and thus epithelial functional integrity. Impairment of the structural and functional integrity may influence recurrence following successful ablation. We aimed to measure the esophageal epithelial intercellular space diameter and MI in the neo-squamous and normal squamous epithelium of patients who underwent successful radiofrequency ablation for dysplastic BE. Methods Forty patients with complete remission of intestinal metaplasia (CRIM) (defined as two negative surveillance endoscopies for intestinal metaplasia) were prospectively recruited. Patients were excluded if they had endoscopic evidence of esophagitis. MI measurements were taken at 1 cm above the GE junction and 2 cm above the prior BE segment (targeting uninvolved squamous epithelium), using a novel through the scope MI probe. Endoscopic biopsies were also taken at these corresponding sites to assess intercellular space diameter using transmission electron microscopy (TEM) using standard techniques. Results 80% of patients were male with a mean age of 69 years. Mean follow since achieving CRIM was 30 months. 39 patients underwent RFA for dysplasia. The mean intercellular space diameter was higher in the neo-squamous epithelium (1.01 μm) when compared to the untreated native squamous epithelium (0.96 μm) [Difference of 0.056 μm, 95% CI of -0.036 to 0.148, P = 0.228]. The mean MI was significantly lower in the neosquamous epithelium (4001.3 Ω) when compared to the untreated native epithelium (5168.1 Ω) [Difference of 1166.7 Ω, 95% CI 418.8 to 1914.6, P = 0.003]. Conclusion Neo-squamous epithelium that replaces BE epithelium following successful endoscopic therapy for BE appears to be functionally and likely structurally deficient with regards to acid reflux barrier function, when compared to native squamous esophageal epithelium. This impairment may be associated with recurrence following successful ablation. Disclosure All authors have declared no conflicts of interest.

Abstract Background Endoscopic mucosal resection (EMR) can be performed en-bloc in Barrett's esophagus (BE) lesions that are ≤2 cm in size. The true size of a BE lesion may be underestimated under white light endoscopy, limiting the rate of en-bloc resection. Volumetric laser endomicroscopy (VLE) provides high-resolution cross-sectional imaging of BE. A greater number of VLE glands are associated with BE dysplasia and may help predict lesion size. The aim of this study was to determine the association between VLE gland count and outcome of resection. Methods EMR specimens from patients with a history of dysplastic BE were imaged with VLE. EMRs performed on BE lesions ≤2cm in size with intent at en-bloc resection were included. Manual quantification of epithelial glands was performed in blinded fashion. Image visualization enhancement software was used to quantify the surface area occupied by epithelial glands on en-face VLE. Histologic en-bloc (R0) and incomplete (R1) resection of the targeted lesion was defined by the absence and presence of dysplasia and/or cancer at the specimen margins respectively. Results The study sample consisted of 37 EMRs from 31 patients. The mean (SD) size of EMRs was 1.04 (0.37) cm. Pathology showed low-grade dysplasia (N = 12), high-grade dysplasia (N = 19), and intramucosal cancer (N = 6). The en-bloc resection rate was 37.8% (R0: N = 14; R1: N = 23). The mean (SD) number of epithelial glands was 13.0 (6.7) and 28.8 (23.9) for R0 and R1 specimens, respectively, with a statistically significant mean difference of 15.8 glands (95% CI: 2–29, P = 0.02) between the two groups. A gland count of 28 or higher per EMR specimen predicted R1 with 100% sensitivity and 39% specificity (ROC: 0.69). The mean (SD) surface area occupied by epithelial glands in R0 and R1 specimens was 0.98 (1.1) mm2 and 2.3 (2.4) mm2, respectively. There was strong correlation between manual gland counts and epithelial gland surface area (R2: 0.81, P < 0.001). Conclusion A higher number of VLE glands in EMR specimens is associated with a lower en-bloc resection rate suggesting that white-light endoscopy underestimates lesion size and that VLE may have a potential role in lesion margin assessment. Disclosure All authors have declared no conflicts of interest.

SummaryPolymorphonuclear (PMN) leucocytes participate in acute inflammatory pathologies such as acute respiratory distress syndrome (ARDS) following traumatic injury and shock, which also activates the coagulation system systemically. Trauma can prime the PMN nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex for an enhanced respiratory burst, but the relative role of various priming agents in this process remains incompletely understood. We therefore set out to identify mediators of PMN priming during coagulation and trauma-shock and determine whether PMN reactive oxygen species (ROS) generated in this manner could influence organ injury and coagulation. Initial experiments demonstrated that PMN are primed for predominantly extracellular ROS production by products of coagulation, which was abrogated by CD88/C5a receptor(C5aR) inhibition. The importance of this was highlighted further by demonstrating that known PMN priming agents result in fractionally different amounts of extracellular versus intracellular ROS release depending on the agent used. Plasma from trauma patients in haemodynamic shock (n = 10) also primed PMN for extracellular ROS in a C5a-dependent manner, which correlated with both complement alternative pathway activation and thrombin generation. Furthermore, PMN primed by preincubation with products of blood coagulation directly caused loss of endothelial barrier function in vitro that was abrogated by C5aR blockade or NADPH oxidase inhibition. Finally, we show in a murine model of trauma-shock that p47phox knock-out (KO) mice with PMN incapable of generating ROS were protected from inflammatory end-organ injury and activated protein C-mediated coagulopathy. In summary, we demonstrate that trauma-shock and coagulation primes PMN for predominantly extracellular ROS production in a C5a-dependent manner that contributes to endothelial barrier loss and organ injury, and potentially enhances traumatic coagulopathy.

Abstract We present the case of a 56-yr-old right-handed male, after informed consent was obtained, who presented with acute confusion and agitation, on the background of a remote history of an uncomplicated resection of a left parietal grade 2 glioma. Imaging revealed a large, acute right temporal intracerebral hemorrhage (ICH). Standard vascular workup for the cause of the ICH included catheter angiography. No direct cause of the hemorrhage was revealed; however, a high grade parasagittal dural arteriovenous fistula (DAVF) with cortical venous reflux was noted close to the prior craniotomy site. The venous reflux was towards the left hemisphere, but it was hypothesized that similar reflux on the right side may have been present and was not presently evident due to thrombosis. The DAVF was embolized by endovascular means, followed by evacuation of the hematoma. Follow-up angiogram 7 mo later revealed a high-flow, right superior temporal cortical arteriovenous malformation (AVM). The DAVF unfortunately had also progressed. Endovascular occlusion of both lesions was attempted but was not successful. Subsequently, microsurgical resection for both the vascular malformations was performed with careful pre- and intraoperative planning to obtain a successful clinical and angiographic result. In this video, we summarize diagnostic and therapeutic nuances that have broad implications for the workup of ICH and the strategic management of a unique scenario involving a brain AVM and high-grade cranial dural fistula in the same patient. Prior to each procedure, informed consent was obtained from the patient, which includes consent for publication.