Update on the management of gastrointestinal varices

Umesha Boregowda, Chandraprakash Umapathy, Nasir Halim, Madhav Desai, Arpitha Nanjappa, Subramanyeswara Arekapudi, Thimmaiah Theethira, Helen Wong, Marina Roytman, Shreyas Saligram, Umesha Boregowda, Chandraprakash Umapathy, Nasir Halim, Madhav Desai, Arpitha Nanjappa, Subramanyeswara Arekapudi, Thimmaiah Theethira, Helen Wong, Marina Roytman, Shreyas Saligram

Abstract

Cirrhosis of liver is a major problem in the western world. Portal hypertension is a complication of cirrhosis and can lead to a myriad of pathology of which include the development of porto-systemic collaterals. Gastrointestinal varices are dilated submucosal veins, which often develop at sites near the formation of gastroesophageal collateral circulation. The incidence of varices is on the rise due to alcohol and obesity. The most significant complication of portal hypertension is life-threatening bleeding from gastrointestinal varices, which is associated with substantial morbidity and mortality. In addition, this can cause a significant burden on the health care facility. Gastrointestinal varices can happen in esophagus, stomach or ectopic varices. There has been considerable progress made in the understanding of the natural history, pathophysiology and etiology of portal hypertension. Despite the development of endoscopic and medical treatments, early mortality due to variceal bleeding remains high due to significant illness of the patient. Recurrent variceal bleed is common and in some cases, there is refractory variceal bleed. This article aims to provide a comprehensive review of the management of gastrointestinal varices with an emphasis on endoscopic interventions, strategies to handle refractory variceal bleed and newer endoscopic treatment modalities. Early treatment and improved endoscopic techniques can help in improving morbidity and mortality.

Keywords: Ectopic varices; Endoscopy; Esophageal varices; Gastric varices; Portal hypertension.

Conflict of interest statement

Conflict-of-interest statement: None of the authors have any conflicts of interest.

Figures

Figure 1
Figure 1
Mechanism of portal hypertension and the development of gastrointestinal varices. VEGF: Vascular endothelial growth factor; PDGF: Platelet-derived growth factor; NO: Nitric oxide; HVPG: Hepatic venous pressure gradient.
Figure 2
Figure 2
Mechanism of variceal bleeding. P: Pressure; R: Radius; WT: Wall thickness.
Figure 3
Figure 3
Screening endoscopy for esophageal varices per practice society guidelines[38,48]. NSBBs: Nonselective beta-blockers; EVL: Endoscopic variceal ligation; EGD: Esophago-gastro duodenoscopy; LS: Liver stiffness; PLT: Platelet.
Figure 4
Figure 4
Endoscopic variceal ligation for primary prophylaxis. A: Esophageal varices before banding; B: Esophageal varix post banding.
Figure 5
Figure 5
Bleeding esophageal varices.
Figure 6
Figure 6
High-risk stigmata of bleeding from esophageal varices. A: Platelet-fibrin plug on esophageal varix (white nipple sign); B: Bleeding esophageal varix post banding.
Figure 7
Figure 7
Endoscopic variceal band ligation.
Figure 8
Figure 8
Metal stents for the treatment of bleeding esophageal varices. A: Bleeding esophageal varix before stenting; B: Esophageal varix after metal stent.
Figure 9
Figure 9
Sarin classification of gastric varices. GOV1: Gastroesophageal varix type 1; GOV2: Gastroesophageal varix type 2; IGV1: Isolated gastric varix type 1; IGV2: Isolated gastric varix type 2.
Figure 10
Figure 10
Gastric varices.
Figure 11
Figure 11
Algorithm for the management of acute variceal bleed. ICU: Intensive care unit; EGD: Esophago-gastro duodenoscopy; NSBB: Nonselective beta blockers; EVL: Endoscopic variceal ligation; TIPS: Transjugular intrahepatic portosystemic shunt.

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Source: PubMed

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