cardiovascular-agents and Esophageal-and-Gastric-Varices

According to their location, gastric varices (GV) are classified as gastroesophageal varices and isolated gastric varices. This review will mainly focus on those GV located in the fundus of the stomach (isolated gastric varices 1 and gastroesophageal varices 2). The 1-year risk of GV bleeding has been reported to be around 10%-16%. Size of GV, presence of red signs, and the degree of liver dysfunction are independent predictors of bleeding. Limited data suggest that tissue adhesives, mainly cyanoacrylate (CA), may be effective and better than propranolol in preventing bleeding from GV. General management of acute GV bleeding must be similar to that of esophageal variceal bleeding, including prophylactic antibiotics, a careful replacement of volemia, and early administration of vasoactive drugs. Small sample-sized randomized controlled trials have shown that tissue adhesives are the therapy of choice for acute GV bleeding. In treatment failures, transjugular intrahepatic portosystemic shunt (TIPS) is considered the treatment of choice. After initial hemostasis, repeated sessions with CA injections along with nonselective beta-blockers are recommended as secondary prophylaxis; whether CA is superior to TIPS in this scenario is not completely clear. Balloon-occluded retrograde transvenous obliteration (BRTO) has been introduced as a new method to treat GV. BRTO is also effective and has the potential benefit of increasing portal hepatic blood flow and therefore may be an alternative for patients who may not tolerate TIPS. However, BRTO obliterates spontaneous portosystemic shunts, potentially aggravating portal hypertension and its related complications. The role of BRTO in the management of acute GV bleeding is promising but merits further evaluation.

Topics: Anti-Bacterial Agents; Balloon Occlusion; Cardiovascular Agents; Cyanoacrylates; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Portasystemic Shunt, Transjugular Intrahepatic; Propranolol; Tissue Adhesives

Acute variceal bleeding (AVB) is the most common cause of upper gastrointestinal hemorrhage in patients with cirrhosis. Advances in the management of AVB have resulted in decreased mortality. To minimize mortality, a multidisciplinary approach addressing airway safety, prompt judicious volume resuscitation, vasoactive and antimicrobial pharmacotherapy, and early endoscopy to obliterate varices is necessary. Placement of a transjugular intrahepatic portosystemic shunt (TIPS) has been used as rescue therapy for patients failing initial attempts at hemostasis. Patients who have a high likelihood of failing initial attempts at hemostasis may benefit from a more aggressive approach using TIPS earlier in their management.

Topics: Acute Disease; Anti-Bacterial Agents; Blood Transfusion; Cardiovascular Agents; Combined Modality Therapy; Endoscopy, Gastrointestinal; Esophageal and Gastric Varices; Humans; Intubation, Intratracheal; Ligation; Portasystemic Shunt, Transjugular Intrahepatic; Risk Factors

Cirrhosis results in portal hypertension in many patients. The major complications of portal hypertension include development of ascites and esophageal or gastric varices. Varices lead to hemorrhage and death in a significant proportion of patients. This review focuses on the pharmacologic approach to management of portal hypertension in patients at risk of variceal hemorrhage, or those who have already had variceal bleeding. Pharmacologic therapy is used for 1) primary prevention of bleeding, 2) management of acute bleeding, and 3) prevention of recurrent bleeding (secondary prophylaxis). For acute esophageal variceal hemorrhage, a variety of pharmacologic agents are used, including somatostatin, octreotide, vapreotide, lanreotide, terlipressin, and vasopressin (with nitrates). For primary and secondary prevention of esophageal variceal hemorrhage, beta-blockers remain the mainstay therapy.

Topics: Adrenergic beta-Antagonists; Algorithms; Antihypertensive Agents; Cardiovascular Agents; Esophageal and Gastric Varices; Esophagoscopy; Gastrointestinal Hemorrhage; Hemostatics; Humans; Hypertension, Portal; Ligation; Liver Cirrhosis; Nitrates; Portasystemic Shunt, Transjugular Intrahepatic; Recurrence; Sclerotherapy; Somatostatin; Vasoconstrictor Agents; Vasopressins

Portal hypertension is a frequent and dangerous consequence of chronic liver diseases. The most important complications are ascites and variceal bleeding. In this article new pathophysiological theories of portal hypertension are reviewed. In addition, the prophylactic and therapeutic management of variceal bleeding are discussed.

Topics: Adrenergic beta-Antagonists; Cardiovascular Agents; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Portasystemic Shunt, Surgical; Sclerotherapy

Pharmacological prophylaxis and the therapy of complications of portal hypertension have recently been attracting more attention. This especially holds true for gastroesophageal variceal bleeding. Vasoconstrictors such as vasopressin, somatostatin, and beta-blockers, as well as vasodilators such as organic nitrates, alpha 2-adrenergic agonists and serotonin-antagonists, are currently used in clinical settings. The aim of this article is to delineate the present pathophysiological concepts accounting for the hemodynamic changes in animal models and patients with portal hypertension, and to summarize the mechanisms of action of the most frequently used pharmacological agents.

Topics: Adrenergic alpha-Agonists; Adrenergic beta-Antagonists; Cardiovascular Agents; Esophageal and Gastric Varices; Hemodynamics; Humans; Hypertension, Portal; Somatostatin; Vasoconstrictor Agents; Vasodilator Agents