80: Management of upper gastrointestinal hemorrhage related to portal hypertension


CHAPTER 80
Management of upper gastrointestinal hemorrhage related to portal hypertension


Patrick S. Kamath and Louis-Michel Wong Kee Song


Mayo Clinic College of Medicine and Science, Rochester, MN, USA


Portal hypertension is defined as an increase in hepatic sinusoidal pressure as measured by a hepatic venous pressure gradient (HVPG) of 6 mmHg or greater.


Portal hypertension results from an increase in and/or resistance to portal blood flow. The anatomy of the portal venous system is shown in Figure 80.1. The increase in portal blood flow is related to vasoactive factors, predominantly nitric oxide (NO) and endothelin‐1 (Figure 80.2). As a means of decompressing the high‐pressure portal venous system, portosystemic collaterals develop at sites where veins from the portal venous system are in proximity to systemic veins, such as at the gastroesophageal junction (Figure 80.3).


Ultrasound imaging can demonstrate an irregular surface of the liver in cirrhosis and portal vein thrombosis, but computed tomography (CT) scan is preferred in patients with portal vein thrombosis to differentiate bland thrombosis (Figure 80.4a) from tumor thrombosis (Figure 80.4b).


Variceal bleed occurs most commonly in the palisade zone of the gastroesophageal junction (Figure 80.5). Esophageal varices may be identified at upper endoscopy as small if <5 mm diameter (Figure 80.6a) or large if >5 mm diameter (Figure 80.6b).


Endoscopic signs associated with an increased risk of bleeding include large varices with red wale marks, cherry red spots, and hematocystic spots (Figure 80.7). Endoscopic variceal ligation (Figure 80.8) or nonselective β‐blockers may be used to prevent bleeding from esophageal varices. Following obliteration of the varices, mucosal scars may be visible (Figure 80.8d). In the long term, esophageal strictures may be a complication. The management algorithm for primary prophylaxis is shown in Figure 80.9.


In patients with recent gastrointestinal bleeding, active bleeding from a varix or a large fibrin plug on an esophageal varix (Figure 80.10) identifies the varix as the source of bleeding. Variceal ligation is carried out to control variceal bleeding and prevent rebleeding (Figure 80.11). Bleeding may also be caused from postvariceal ligation ulcers (Figure 80.12a) which may be treated with hemostatic powder application (Figure 80.12b). A Minnesota tube (Figure 80.13a), esophageal self‐expandable metal stents (Figure 80.14) or transjugular intrahepatic portosystemic shunt (TIPS) (Figure 80.15) are used when pharmacological and endoscopic treatments are unable to control the bleed. The management algorithm for control of acute esophageal variceal bleeding is shown in Figure 80.16.


The classification of gastric varices is shown in Figure 80.17. Actively bleeding GOV type 1 varices may be banded to provide hemostatic control (Figure 80.18). Isolated gastric varices are shown in Figure 80.19. The optimal treatment for control of gastric variceal bleeding is cyanoacrylate glue injection into the gastric varix (Figure 80.20a–c). Follow‐up endoscopy may show a glue cast (Figure 80.20d,e).


In the presence of a gastro–renal shunt, balloon‐occluded retrograde transvenous obliteration of gastric varices may be carried out (Figure 80.21). The presence of a gastro–renal shunt places patients who have bled from fundal varices at risk for distal glue embolization in the lungs and brain. In such situations, angiographic balloon occlusion of the shunt is carried out prior to endoscopic cyanoacrylate glue injection (Figure 80.22). The suggested algorithm for management of acute gastric variceal bleeding is outlined in Figure 80.23.


Bleeding may also occur from mucosal lesions in the stomach. Mild portal hypertensive gastropathy (Figure 80.24a,b) is demonstrated by a mosaic pattern of the mucosa, whereas the presence of red signs characterizes severe portal hypertensive gastropathy (Figure 80.24c) which places patients at risk for bleeding. Gastric vascular ectasia arranged in a linear pattern in the antrum (watermelon stomach) (Figure 80.25a,b) may be treated with argon plasma coagulation (Figure 80.25c). The vascular ectasia may also be more diffuse (Figure 80.26). Hyperplastic polypoid lesions, which may follow argon plasma coagulation for gastric antral vascular ectasia and can be a source of chronic blood loss, are shown in Figure 80.27a. These lesions may be treated by hot snare resection (Figure 80.27b). Radiofrequency ablation is another technique for treating gastric vascular ectasia (Figure 80.28). Nodular forms of gastric antral vascular ectasia may be refractory to argon plasma coagulation and require band ligation (Figure 80.29).


Ectopic varices occur at sites other than the gastroesophageal junction and may be treated by band ligation, clips, or glue therapy (Figure 80.30).

Schematic illustration of the anatomy of the portal venous system is shown.

Figure 80.1 The anatomy of the portal venous system is shown. The portal vein is formed by the confluence of the splenic vein and the superior mesenteric vein.

Schematic illustration of pathophysiology of portal hypertension.

Figure 80.2 Pathophysiology of portal hypertension. Portal hypertension results from a combination of increased portal blood flow and increased resistance to portal blood flow. The increase in intrahepatic resistance has a fixed component as well as a variable component. ET1 is a vasoconstrictor; the other molecules are vasodilators. CO, carbon monoxide; ET1, endothelin‐1; eNOS, endothelial nitric oxide synthase; NO, nitric oxide; TNF, tumor necrosis factor; VEGF, vascular endothelial growth factor.

Schematic illustration of (a,b) a means of decompressing the high-pressure portal venous system, portosystemic collaterals develop at sites where veins from the portal venous system are in proximity to systemic veins, such as at the gastroesophageal junction
Schematic illustration of (a,b) a means of decompressing the high-pressure portal venous system, portosystemic collaterals develop at sites where veins from the portal venous system are in proximity to systemic veins, such as at the gastroesophageal junction

Figure 80.3 (a,b) As a means of decompressing the high‐pressure portal venous system, portosystemic collaterals develop at sites where veins from the portal venous system are in proximity to systemic veins, such as at the gastroesophageal junction.

Image described by caption.

Figure 80.4 (a) CT abdomen demonstrating acute portal vein thrombosis identified by central lucency (arrowheads), expanded vein, and contrast at the periphery of the vein. Note the absence of portosystemic collaterals, which are seen in chronic portal vein thrombosis. (b) CT abdomen showing tumor thrombus identified by arterialization of the portal vein thrombus (arrowheads). Tumor portal vein thrombosis is characterized by the “threads and streaks” sign, which results from arterioles supplying the tumor in the portal vein.

Schematic illustration of venous drainage of the gastroesophageal junction (GEJ).

Figure 80.5

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Nov 27, 2022 | Posted by in GASTROENTEROLOGY | Comments Off on 80: Management of upper gastrointestinal hemorrhage related to portal hypertension
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