Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are 2 distinct gastric vascular abnormalities that may present with acute or chronic blood loss. PHG requires the presence of portal hypertension and is typically associated with chronic liver disease, whereas there is controversy about the association of GAVE with chronic liver disease and/or portal hypertension. Distinguishing between GAVE and PHG is crucial because their treatment strategies differ. This review highlights characteristic endoscopic appearances and the clinical features of PHG and GAVE, which, in turn, aid in their appropriate management.

Gastric antral vascular ectasia (GAVE) is a rare cause of upper gastrointestinal bleeding associated with cirrhosis. The first-line treatment is endoscopic therapy with argon plasma coagulation (APC). There is a high recurrence rate, but some evidence suggests that thalidomide could play an important role in controlling refractory anaemia due to GAVE. The authors present the case of a cirrhotic patient with a recent diagnosis of GAVE, who underwent multiple endoscopic treatments and blood transfusions because of haematemesis. The patient started thalidomide and 6 months later, there was no recurrence of haematemesis and haemoglobin levels were stable, with no reported adverse effects.

The chronic bleeding associated with gastric antral vascular ectasia (GAVE) presenting with cirrhosis is more severe than that associated with portal hypertensive gastropathy.Argon plasma coagulation remains the first-line treatment, but GAVE has a high recurrence rate.Thalidomide could be an effective and safe option for recurrent bleeding due to GAVE in patients with cirrhosis.

More than five decades after it was originally conceptualized as rescue therapy for patients with intractable variceal bleeding, the transjugular intrahepatic portosystemic shunt (TIPS) procedure continues to remain a focus of intense clinical and biomedical research. By the impressive reduction in portal pressure achieved by this intervention, coupled with its minimally invasive nature, TIPS has gained increasing acceptance in the treatment of complications of portal hypertension. The early years of TIPS were plagued by poor long-term patency of the stents and increased incidence of hepatic encephalopathy. Moreover, the diversion of portal flow after placement of TIPS often resulted in derangement of hepatic functions, which was occasionally severe. While the incidence of shunt dysfunction has markedly reduced with the advent of covered stents, hepatic encephalopathy and instances of early liver failure continue to remain a significant issue after TIPS. It has emerged over the years that careful selection of patients and diligent post-procedural care is of paramount importance to optimize the outcome after TIPS. The past twenty years have seen multiple studies redefining the role of TIPS in the management of variceal bleeding and refractory ascites while exploring its application in other complications of cirrhosis like hepatic hydrothorax, portal hypertensive gastropathy, ectopic varices, hepatorenal and hepatopulmonary syndromes, non-tumoral portal vein thrombosis and chylous ascites. It has also been utilized to good effect before extrahepatic abdominal surgery to reduce perioperative morbidity and mortality. The current article aims to review the updated literature on the status of TIPS in the management of patients with liver cirrhosis.

Bleeding occurs with some regularity at the end of life. Patients often endure fatigue, weakness, pain, dyspnea and anxiety. These symptoms are magnified in visually apparent bleeds. Management can be particularly challenging as we attempt to balance therapies with goals of care. Children are at risk for such complications and symptoms; providers must ensure comfort for both the patient and family.

A 7-year-old male with recurrent, refractory Burkitt lymphoma was frequently hospitalized for palliative chemotherapy and disease complications. On his final admission, he experienced gross hemoptysis and hematemesis: he was short of breath, fatigued and anxious due to his blood loss. His and his family's angst were heightened by "seeing" his bleed. Potential, especially invasive, treatments were limited by our goals to promote comfort, limit interventions, maintain alertness, poor intravenous access and a small bowel obstruction. Nebulized vasopressin, 10 units in 4ml of normal saline given over 10 minutes provided JC with needed relief. His bleeding remitted and he tolerated its administration.

There are many treatments for hemorrhage; however, given the challenges of goals of care, administration, side-effects and tolerability, further investigation into nebulized vasopressin as a potential therapy for hemoptysis and hematemesis at the end-of-life is warranted.

Thalidomide was initially synthesised in 1954 and marketed as a sedative and antiemetic for morning sickness. It was withdrawn in 1961 due to the realisation that it was teratogenic with over 10 000 children born with congenital abnormalities. Since then it has been used for treatment of dermatological and oncological conditions, including myeloma. In 1994, it was found to have a potent antiangiogenic effect via downregulation of vascular endothelial growth factor (VEGF). This has led to its use in gastrointestinal bleeding, as vascular abnormalities such as angiodysplasia have been found to have elevated VEGF levels. This article will review the current evidence of the use of thalidomide in bleeding associated with gastrointestinal vascular malformations, including angiodysplasia, gastric cancer and radiation-induced proctitis.

Portal hypertensive gastropathy (PHG) is a painless condition of gastric mucosal ectasia and impaired mucosal defense, commonly seen in patients with elevated portal pressures. While it is typically asymptomatic and incidentally discovered on upper endoscopy, acute and chronic bleeding may occur. There are no definitive recommendations for treatment of asymptomatic PHG. Non-selective β-blockers represent the mainstay of therapy for chronic bleeding, while somatostatin and vasopressin and their derivatives may be used in conjunction with supportive measures for acute bleeding. Salvage therapy with transjugular intrahepatic portosystemic shunt or rarely surgical shunt is appropriate when medical management fails. The role of endoscopic therapy for PHG is controversial. Liver transplantation should be considered as a final resort in cases of refractory bleeding due to PHG.

Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are gastric mucosal lesions that mostly present as chronic anemia and rarely cause the acute gastrointestinal hemorrhage. Despite similar clinical manifestations, their pathophysiology and management are entirely different. PHG is seen exclusively in patients with portal hypertension, but GAVE can also be observed in patients with other conditions. Their diagnosis is endoscopic, and although generally each of them has a characteristic endoscopic appearance and distribution, there are cases in which the differential is difficult and must rely on histology. This review focuses on the management of both entities. The mainstay of management of PHG is based on portal-hypotensive pharmacological treatment while GAVE benefits from hormonal therapy, endoscopic Nd:YAG laser, and argon plasma coagulation. More invasive options should be reserved for refractory cases.

Portal hypertensive gastropathy and gastric antral vascular ectasia are gastric mucosal lesions that can cause chronic gastrointestinal haemorrhage and, consequently, chronic anaemia, in patients with cirrhosis. Although chronic anaemia is the most common clinical manifestation, these entities may also lead to acute gastrointestinal bleeding. Despite similar clinical manifestations, their pathophysiology and management are entirely different. Their diagnosis is endoscopic and although generally each of them has a characteristic endoscopic appearance and distribution, there are cases in which the differential is difficult and must rely on histology. This review focuses on the management of both entities. The mainstay of management of portal hypertensive gastropathy is based on portal-hypotensive pharmacological treatment whilst gastric antral vascular ectasia benefits from endoscopic therapy. More invasive options should be reserved for refractory cases.

Portal hypertensive gastropathy and gastric antral vascular ectasia may cause gastrointestinal hemorrhage in patients with portal hypertension. Whereas the former presents exclusively in patients with portal hypertension, gastric antral vascular ectasia can also be observed in patients with other conditions. Diagnosis is established with upper gastrointestinal endoscopy, although some cases may require a biopsy to confirm the diagnosis. The most frequent manifestation is ferropenic anemia, which may become transfusion dependent. Treatment in portal hypertensive gastropathy is focused on portal pressure reducing drugs, mainly nonselective beta-blockers, whereas in gastric antral vascular ectasia treatment is based on endoscopic ablation. More invasive options can be used if first-line therapies fail, although these should be evaluated on a case-by-case basis.

Medical management of severe gastrointestinal bleeding can present a therapeutic challenge. We describe a case of bleeding secondary to gastric cancer that failed to settle, despite treatment with tranexamic acid, etamsylate and sucralfate. Thalidomide was prescribed for its antiangiogenic properties. Bleeding settled within 1 week of starting 300 mg of thalidomide nocte. The effect appeared to be dose dependent, with bleeding recurring only when the dose was reduced to 100 mg of thalidomide nocte.