Despite improvements in endoscopic technologies and accessories, development of advanced endoscopy fellowship programs, and advances in ancillary imaging techniques, biliary cannulation in endoscopic retrograde cholangiopancreatography (ERCP) can still be unsuccessful in up to 20% of patients, even in referral centers. Once cannulation has been deemed to be difficult, the risk of post-ERCP pancreatitis and technical failure inherently increases. A number of factors, including endoscopist experience and patient anatomy, have been associated with difficult biliary cannulation, but predicting a case of difficult cannulation a priori is often not possible. Numerous techniques such as pancreatic guidewire and stenting, early pre-cut, and rendezvous may be employed when standard approaches fail. Data regarding the rate of success and adverse events of these techniques have been variable, though most studies suggest that pancreatic duct stenting generally reduces the rate of post-ERCP pancreatitis in instances of difficult biliary cannulation. Here we provide a review on difficult biliary cannulation and discuss how the choice of which techniques to employ and how to best employ them should be individualized and take into account the skill of the endoscopist, the disorder being treated, the anatomy of the patient, and the available biomedical literature.
Hemobilia refers to bleeding from and/or into the biliary tract and is an uncommon but important cause of gastrointestinal hemorrhage. Reports of hemobilia date back to the 1600s, but due to its relative rarity and challenges in diagnosis, only in recent decades has hemobilia been more critically studied. The majority of cases of hemobilia are iatrogenic and caused by invasive procedures involving the liver, pancreas, bile ducts and/or the hepatopancreatobiliary vasculature, with trauma and malignancy representing the two other leading causes. A classic triad of right upper quadrant pain, jaundice, and overt upper gastrointestinal bleeding has been described (i.e. Quincke’s triad), but this is present in only 25%–30% of patients with hemobilia. Therefore, prompt diagnosis depends critically on having a high index of suspicion, which may be based on a patient’s clinical presentation and having recently undergone (peri-) biliary instrumentation or other predisposing factors. The treatment of hemobilia depends on its severity and suspected source and ranges from supportive care to advanced endoscopic, interventional radiologic, or surgical intervention. Here we provide a clinical overview and update regarding the etiology, diagnosis, and treatment of hemobilia geared for specialists and subspecialists alike.
Hemobilia refers to macroscopic blood in the lumen of the biliary tree. It represents an uncommon, but important, cause of gastrointestinal bleeding and can have potentially lethal sequelae if not promptly recognized and treated. The earliest known reports of hemobilia date to the 17th century, but due to the relative rarity and challenges in diagnosis of hemobilia, it has historically not been well‐studied. Until recently, most cases of hemobilia were due to trauma, but the majority now occur as a sequela of invasive procedures involving the hepatopancreatobiliary system. A triad (Quincke's) of right upper quadrant pain, jaundice and overt gastrointestinal bleeding has been classically described in hemobilia, but it is present in only a minority of patients. Therefore, prompt diagnosis depends critically on a high index of suspicion based on a patient's clinical presentation and a history of recently undergoing hepatopancreatobiliary intervention or having other predisposing factors. Treatment of hemobilia depends on the suspected source and clinical severity and thus ranges from supportive medical care to urgent advanced endoscopic, interventional radiologic, or surgical intervention. In the present review, we provide a historical perspective, clinical update and overview of current trends and practices pertaining to hemobilia.
Hemobilia refers to bleeding from and/or into the biliary tract and is an uncommon cause of gastrointestinal hemorrhage. Hemobilia has been documented since the 1600s, but due to its relative rarity, it has only been more critically examined in recent decades. Most cases of hemobilia are iatrogenic and caused by procedures involving the liver, pancreas, bile ducts, and/or the hepatopancreatobiliary vasculature, with trauma and malignancy representing the two other major causes. A classic triad of right upper quadrant pain, jaundice, and overt upper gastrointestinal bleeding has been described, but this is present in only 25–30% of patients with hemobilia. Historically, the gold standard for diagnosis and treatment has been angiography and interventional radiologic intervention, respectively. However, the paradigm is shifting, at least in select cases, towards first-line reliance on noninvasive imaging (e.g., computed tomography) and therapeutic endoscopy, owing to advances in and the less invasive nature of both, while saving interventional radiological and/or surgical intervention for refractory or imminently life-threatening cases.
Histone acetylation is a key component in the consolidation of long-term fear memories. Histone acetylation is fueled by acetyl-coenzyme A (acetyl-CoA), and recently, nuclear-localized metabolic enzymes that produce this metabolite have emerged as direct and local regulators of chromatin. In particular, acetyl-CoA synthetase 2 (ACSS2) mediates histone acetylation in the mouse hippocampus. However, whether ACSS2 regulates long-term fear memory remains to be determined. Here, we show that Acss2 knockout is well tolerated in mice, yet the Acss2-null mouse exhibits reduced acquisition of long-term fear memory. Loss of Acss2 leads to reductions in both histone acetylation and expression of critical learning and memory-related genes in the dorsal hippocampus, specifically following fear conditioning. Furthermore, systemic administration of blood–brain barrier–permeable Acss2 inhibitors during the consolidation window reduces fear-memory formation in mice and rats and reduces anxiety in a predator-scent stress paradigm. Our findings suggest that nuclear acetyl-CoA metabolism via ACSS2 plays a critical, previously unappreciated, role in the formation of fear memories.
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