Abstract
This chapter discusses the developmental and pathophysiological mechanisms of portal hypertension and the consequent formation of esophagogastric varices. Anatomical and pathophysiological findings regarding the diagnosis and treatment of varices can provide useful information for clinical practice. In addition, hemodynamic changes caused by treatment are also described. Endoscopic treatment is well indicated for esophagogastric varices, irrespective of urgent, elective, or prophylactic purposes. As an endoscopic treatment-resistant condition, a pipeline stem varix of the esophagus is presented.
Among gastric varices, acutely bleeding large isolated gastric fundal varices (IGFVs) that do not communicate with esophageal varices are resistant to endoscopic treatment and require the use of n-butyl-2-cyanoacrylate (tissue adhesive glue) injection for hemostasis. Patients with large IGFVs often have portosystemic shunts, mainly splenorenal (S-R) shunts, and are prone to recurrent hepatic encephalopathy.
Balloon-occluded retrograde transvenous obliteration (B-RTO), a procedure developed in Japan, can totally eradicate large IGFVs with S-R shunts. With major shunt obliteration achieved, B-RTO is also markedly effective against shunt encephalopathy. Portosystemic shunt syndrome (portosystemic shuntopathy), which has been defined based on accumulated B-RTO case data, is also described herein.
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Toyonaga, A. (2019). Mechanism and Pathophysiology of Portal Hypertension. In: Obara, K. (eds) Clinical Investigation of Portal Hypertension. Springer, Singapore. https://doi.org/10.1007/978-981-10-7425-7_5
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DOI: https://doi.org/10.1007/978-981-10-7425-7_5
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