**9. Management of PHG**

The goal of management of PHG is to reduce portal pressure.

## **9.1. Primary prophylaxis**

PHG in asymptomatic patients who have no evidence of bleeding is discovered accidentally during screening for either chronic iron deficiency anemia or for esophageal varices in patients with cirrhosis. Till now, there is no recommendation to start any primary prophylaxis to pre‐ vent bleeding from PHG patients, except if there is an indication of beta‐blocker for other rea‐ sons. However, in asymptomatic patients with both esophageal varices and PHG, if the patient undergoes esophageal eradication therapy, co‐administration of a nonselective beta‐blocker is beneficial. The dose of beta blocker should be titrated to a goal heart rate of 55–60 bpm or a 25% reduction from baseline. On the other hand, in patients with severe PHG and no varices, starting prophylaxis therapy with nonselective beta‐blockers, should be considered. Yet, this approach is controversial, and more research is needed to clarify the prophylactic role of beta‐ blockers as primary prophylaxis for bleeding from PHG [34].

#### **9.2. Secondary prophylaxis**

Beta‐blockers (like propranolol or nadolol) are used as secondary prophylaxis, and are the basis of therapy, to prevent recurrent bleeding from PHG. It is not only used to prevent the bleeding, but it also improves the severity score of PHG by endoscopy, changing it from severe to mild, or even completely curing it. On the other hand, about 50% of PHG patients especially cirrhotic dur‐ ing a 2‐year follow up, show mild or even no response to beta blocker therapy. For those patients adding isosorbide 5‐mononitrate may have a synergistic effect to reduce the portal pressure [37].

Addition of beta‐blocker therapy to endoscopic management of varices is beneficial in reduc‐ ing the progression of PHG after endoscopic therapy of varices. Propranolol, a non‐selective beta‐blocker (24–480 mg/day), has been commonly used in these cases. The dose of proprano‐ lol should be increased gradually to maximum dose (up to 160 mg twice daily) with targeted heart rate of 55–60 bpm, and should be continued as long as there is portal hypertension [37]. In patients with iron deficiency anemia, iron replacement therapy and beta blocker should be started simultaneously.

#### **9.3. Treatment of chronic bleeding**

Patients with PHG with or without cirrhosis, and chronic blood loss are commonly presented with iron deficiency anemia. Thorough investigation of these patients must be done to rule out other causes of iron deficiency anemia before attributing PHG as the cause. All patients with PHG and iron deficiency anemia should start iron‐replacement therapy either; oral prep‐ arations, or intravenous (IV) iron.

To reduce chronic bleeding from PHG, with or without portal hypertension, portal pressure should be reduced, therefore non selective beta blocker is the first line of treatment. The use of beta blockers has proved efficient, based on both experimental and clinical investigations demonstrating that, propranolol reduces portal pressure and cause vasoconstriction in the overall splanchnic vascular bed.

Anti‐oxidants have also been used to treat PHG. Experimentally, Vitamin E led to complete reversal of susceptibility of PHG mucosa to alcohol injury, in rats. Vitamin E also, led to the restoration of normal Extracellular signal‐regulated kinase (ERK‐2 signaling), which plays a pivotal role in healing after gastric mucosal injury. Thus, vitamin E may have a protective effect on the PHG mucosa [38].

Use of other pharmacological agents such as losartan, thalidomide and corticosteroids have been prescribed in the treatment of chronic bleeding from PHG. However, the evidence sup‐ porting their use in PHG bleeding is weak [39].

#### **9.4. Treatment of acute bleeding**

**9. Management of PHG**

70 Stomach Disorders

**9.1. Primary prophylaxis**

**9.2. Secondary prophylaxis**

started simultaneously.

**9.3. Treatment of chronic bleeding**

arations, or intravenous (IV) iron.

The goal of management of PHG is to reduce portal pressure.

blockers as primary prophylaxis for bleeding from PHG [34].

PHG in asymptomatic patients who have no evidence of bleeding is discovered accidentally during screening for either chronic iron deficiency anemia or for esophageal varices in patients with cirrhosis. Till now, there is no recommendation to start any primary prophylaxis to pre‐ vent bleeding from PHG patients, except if there is an indication of beta‐blocker for other rea‐ sons. However, in asymptomatic patients with both esophageal varices and PHG, if the patient undergoes esophageal eradication therapy, co‐administration of a nonselective beta‐blocker is beneficial. The dose of beta blocker should be titrated to a goal heart rate of 55–60 bpm or a 25% reduction from baseline. On the other hand, in patients with severe PHG and no varices, starting prophylaxis therapy with nonselective beta‐blockers, should be considered. Yet, this approach is controversial, and more research is needed to clarify the prophylactic role of beta‐

Beta‐blockers (like propranolol or nadolol) are used as secondary prophylaxis, and are the basis of therapy, to prevent recurrent bleeding from PHG. It is not only used to prevent the bleeding, but it also improves the severity score of PHG by endoscopy, changing it from severe to mild, or even completely curing it. On the other hand, about 50% of PHG patients especially cirrhotic dur‐ ing a 2‐year follow up, show mild or even no response to beta blocker therapy. For those patients adding isosorbide 5‐mononitrate may have a synergistic effect to reduce the portal pressure [37]. Addition of beta‐blocker therapy to endoscopic management of varices is beneficial in reduc‐ ing the progression of PHG after endoscopic therapy of varices. Propranolol, a non‐selective beta‐blocker (24–480 mg/day), has been commonly used in these cases. The dose of proprano‐ lol should be increased gradually to maximum dose (up to 160 mg twice daily) with targeted heart rate of 55–60 bpm, and should be continued as long as there is portal hypertension [37]. In patients with iron deficiency anemia, iron replacement therapy and beta blocker should be

Patients with PHG with or without cirrhosis, and chronic blood loss are commonly presented with iron deficiency anemia. Thorough investigation of these patients must be done to rule out other causes of iron deficiency anemia before attributing PHG as the cause. All patients with PHG and iron deficiency anemia should start iron‐replacement therapy either; oral prep‐

To reduce chronic bleeding from PHG, with or without portal hypertension, portal pressure should be reduced, therefore non selective beta blocker is the first line of treatment. The use of beta blockers has proved efficient, based on both experimental and clinical investigations


#### **9.5. For refractory cases**

When the patients do not respond to the previously mentioned treatments, invasive interven‐ tion must be done. Transjugular intrahepatic portosystemic shunt (TIPS) or surgical shunt are considered as salvage therapy only when they are performed in certain circumstances and in an expert center due to their significant morbidity and mortality results [41].

Surgical shunting has also proved beneficial in refractory bleeding from PHG however, this benefit is limited by an increase in the risk of deterioration of the hepatic function in patients with cirrhosis. Only cirrhotic patients with Child Pugh score A or B found improved out‐ comes from surgical shunting with reduced mortality. Comparing the results of TIPS with surgical shunt, it is reported that surgical shunt reduced re‐bleeding, with fewer shunt complication e.g. shunt revisions, stent thrombosis, re‐stenosis, and re‐intervention of TIPS. However, long‐term mortality was similar. On the other hand, similar results were found between TIPSS and distal splenorenal shunting with regards to re‐bleeding, enceph‐ alopathy, and survival. Whatever the method of shunting in case of refractory bleeding from PHG, it should always be performed in expertise center. Surgical shunting may be an option only in CTP stage A cirrhosis with PHG or in patients with non‐cirrhotic portal hypertension [42].

**Figure 3.** Treatment algorithm of portal hypertensive gastropathy.

**Argon plasma coagulation (APC)** is an electrosurgical technique used for treatment of bleed‐ ing of PHG. APC is a noncontact thermal coagulation, high frequency current, that is applied to the bleeding site through an argon plasma jet, this creates effective hemostasis and a homog‐ enous surface coagulation with limited depth penetration. Treatment with APC decrease the need of transformation and improve the hemoglobin level in PHG patients, accordingly APC is an effective and rapid therapy to control bleeding from PHG, especially if there is a con‐ traindication for beta blockers. If beta blocker can be used, co administration with APC has a synergistic effect in controlling PHG bleeding [5].

**Hemospray:** In patients with acute active bleeding due to PHG, it may be useful to use hemo‐ static powder that acts as a barrier to enhance the action of the clotting factors, giving time for the coagulation process to act and stop the bleeding [43]. A treatment algorithm for patients with PHG is described in **Figure 3**.

## **10. Mortality rates**

Limited data on mortality due to bleeding from PHG is available, but the bleeding from PHG is rarely fatal. It represents a small percentage if compared with the mortality from other causes of gastrointestinal bleeding due to portal hypertension, and especially in comparison to variceal bleeding. Also, in cirrhotic patients it represents only <1% of the mortality, because the bleeding is typically mild [4]. As bleeding from PHG is an unusual direct cause of death, it does not affect the survival in cirrhotic patients. However, anemia from chronic bleeding or repeated acute bleeding may lead to deterioration of the liver function.
