Atrioesophageal Fistula: A Rare but Dangerous Complication From Catheter Ablation.

Atrioesophageal fistula is a rare complication of catheter ablation. It can be discovered on computerized topography of the chest. It is a difficulty entity to diagnose and treat and carries a mortality between 67% and 100%. Management options include surgical repair and esophageal stenting. We report here a rare case of an atrioesophageal fistula that presented with massive upper gastrointestinal bleeding and hemiparalysis.

Endoscopic therapies for Barrett's esophagus.

The management of Barrett's esophagus (BE) has evolved as newer technologies and novel methods are developed. Endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) are the initial interventions of choice for nodular BE, with ESD reserved for endoscopists highly trained in the technique and for larger lesions that would warrant en bloc resection. Resection should then be followed by ablative therapy, which remains first line in the treatment of BE with dysplasia. Although there is a myriad of ablation techniques available to the endoscopist, this review has found that radiofrequency ablation (RFA) continues to have the most robust safety and efficacy data to support its use despite a relatively high rate of recurrence. Cryotherapy and Hybrid-APC appear to be safe and effective as RFA alternatives, but further trials are still needed to directly compare their outcomes to RFA and ultimately guide changes in treatment decisions.

Acute kidney injury and hepatorenal syndrome in cirrhosis.

Acute kidney injury (AKI) in cirrhosis, including hepatorenal syndrome (HRS), is a common and serious complication in cirrhotic patients, leading to significant morbidity and mortality. AKI is separated into two categories, non-HRS AKI and HRS-AKI. The most recent definition and diagnostic criteria of AKI in cirrhosis and HRS have helped diagnose and prognosticate the disease. The pathophysiology behind non-HRS-AKI and HRS is more complicated than once theorized and involves more processes than just splanchnic vasodilation. The common biomarkers clinicians use to assess kidney injury have significant limitations in cirrhosis patients; novel biomarkers being studied have shown promise but require further studies in clinical settings and animal models. The overall management of non-HRS AKI and HRS-AKI requires a systematic approach. Although pharmacological treatments have shown mortality benefit, the ideal HRS treatment option is liver transplantation with or without simultaneous kidney transplantation. Further research is required to optimize pharmacologic and nonpharmacologic approaches to treatment. This article reviews the current guidelines and recommendations of AKI in cirrhosis.

Single-neuron NMDA receptor phenotype influences neuronal rewiring and reintegration following traumatic injury.

Alterations in the activity of neural circuits are a common consequence of traumatic brain injury (TBI), but the relationship between single-neuron properties and the aggregate network behavior is not well understood. We recently reported that the GluN2B-containing NMDA receptors (NMDARs) are key in mediating mechanical forces during TBI, and that TBI produces a complex change in the functional connectivity of neuronal networks. Here, we evaluated whether cell-to-cell heterogeneity in the connectivity and aggregate contribution of GluN2B receptors to [Ca(2+)]i before injury influenced the functional rewiring, spontaneous activity, and network plasticity following injury using primary rat cortical dissociated neurons. We found that the functional connectivity of a neuron to its neighbors, combined with the relative influx of calcium through distinct NMDAR subtypes, together contributed to the individual neuronal response to trauma. Specifically, individual neurons whose [Ca(2+)]i oscillations were largely due to GluN2B NMDAR activation lost many of their functional targets 1 h following injury. In comparison, neurons with large GluN2A contribution or neurons with high functional connectivity both independently protected against injury-induced loss in connectivity. Mechanistically, we found that traumatic injury resulted in increased uncorrelated network activity, an effect linked to reduction of the voltage-sensitive Mg(2+) block of GluN2B-containing NMDARs. This uncorrelated activation of GluN2B subtypes after injury significantly limited the potential for network remodeling in response to a plasticity stimulus. Together, our data suggest that two single-cell characteristics, the aggregate contribution of NMDAR subtypes and the number of functional connections, influence network structure following traumatic injury.

Dynamic changes in neural circuit topology following mild mechanical injury in vitro.

Despite its enormous incidence, mild traumatic brain injury is not well understood. One aspect that needs more definition is how the mechanical energy during injury affects neural circuit function. Recent developments in cellular imaging probes provide an opportunity to assess the dynamic state of neural networks with single-cell resolution. In this article, we developed imaging methods to assess the state of dissociated cortical networks exposed to mild injury. We estimated the imaging conditions needed to achieve accurate measures of network properties, and applied these methodologies to evaluate if mild mechanical injury to cortical neurons produces graded changes to either spontaneous network activity or altered network topology. We found that modest injury produced a transient increase in calcium activity that dissipated within 1 h after injury. Alternatively, moderate mechanical injury produced immediate disruption in network synchrony, loss in excitatory tone, and increased modular topology. A calcium-activated neutral protease (calpain) was a key intermediary in these changes; blocking calpain activation restored the network nearly completely to its pre-injury state. Together, these findings show a more complex change in neural circuit behavior than previously reported for mild mechanical injury, and highlight at least one important early mechanism responsible for these changes.