• esophageal varices
• gastrointestinal bleeding
• liver cirrhosis
• lower gastrointestinal bleeding
• peptic ulcer bleeding

• Humans
• Male
• Female
• Gastrointestinal Hemorrhage/etiology
• Gastrointestinal Hemorrhage/mortality
• Middle Aged
• Retrospective Studies
• Liver Cirrhosis/complications
• Liver Cirrhosis/mortality
• Aged
• Esophageal and Gastric Varices/complications
• Adult
• Hemorrhoids/complications
• Hospitalization/statistics & numerical data
• Case-Control Studies
• Stomach Ulcer/complications
• Duodenal Ulcer/complications
• Risk Factors

• Acute hematochezia
• Clipping therapy
• Coagulation therapy
• Colonic angioectasia
• Rebleeding

Acute non-variceal bleeding accounts for approximately 20% of all-cause bleeding episodes in patients with liver cirrhosis. It is associated with high morbidity and mortality therefore prompt diagnosis and endoscopic management are crucial.

To evaluate available data on the efficacy of endoscopic treatment modalities used to control acute non-variceal gastrointestinal bleeding (GIB) in cirrhotic patients as well as to assess treatment outcomes.

Employing PRISMA methodology, the MEDLINE was searched through PubMed using appropriate MeSH terms. Data are reported in a summative manner and separately for each major non-variceal cause of bleeding.

Overall, 23 studies were identified with a total of 1288 cirrhotic patients of whom 958/1288 underwent endoscopic therapy for acute non-variceal GIB. Peptic ulcer bleeding was the most common cause of acute non-variceal bleeding, followed by portal hypertensive gastropathy, gastric antral vascular ectasia, Mallory-Weiss syndrome, Dieaulafoy lesions, portal hypertensive colopathy, and hemorrhoids. Failure to control bleeding from all-causes of non-variceal GIB accounted for less than 3.5% of cirrhotic patients. Rebleeding (range 2%-25%) and mortality (range 3%-40%) rates varied, presumably due to study heterogeneity. Rebleeding was usually managed endoscopically and salvage therapy using arterial embolisation or surgery was undertaken in very few cases. Mortality was usually associated with liver function deterioration and other organ failure or infections rather than uncontrolled bleeding. Endoscopic treatment-related complications were extremely rare. Lower acute non-variceal bleeding was examined in two studies (197/1288 patients) achieving initial hemostasis in all patients using argon plasma coagulation for portal hypertensive colopathy and endoscopic band ligation or sclerotherapy for bleeding hemorrhoids (rebleeding range 10%-13%). Data on the efficacy of endoscopic therapy of cirrhotic patients vs non-cirrhotic controls with acute GIB are very scarce.

Endotherapy seems to be efficient as a means to control non-variceal hemorrhage in cirrhosis, although published data are very limited, particularly those comparing cirrhotics with non-cirrhotics and those regarding acute bleeding from the lower gastrointestinal tract. Rebleeding and mortality rates appear to be relatively high, although firm conclusions may not be drawn due to study heterogeneity. Hopefully this review may stimulate further research on this subject and help clinicians administer optimal endoscopic therapy for cirrhotic patients.

• Liver cirrhosis
• Non-variceal gastrointestinal hemorrhage
• Gastrointestinal endoscopy
• Endoscopic therapy
• Patient outcomes
• Peptic ulcer
• Mallory Weiss syndrome
• Gastric antral vascular ectasia

The more modern and accurate concept of a rebalanced hemostatic status in cirrhosis is slowly replacing the traditional belief of patients with cirrhosis being “auto-anticoagulated”, prone only to bleeding complications, and protected from thrombotic events. With greater attention to clinical thrombotic events, their impact on the natural history of cirrhosis, and with the emergence and increased use of point-of-care and global assays, it is now understood that cirrhosis results in profound hemostatic alterations that can lead to thrombosis as well as to bleeding complications. Although many clinical decisions are still based on traditional coagulation parameters such as prothrombin (PT), PT, and international normalized ratio, it is increasingly recognized that these tests do not adequately predict the risk of bleeding, nor they should guide pre-emptive interventions. Moreover, altered coagulation tests should not be considered as a contraindication to the use of anticoagulation, although this therapeutic or prophylactic approach is not at present routinely undertaken. Gastroesophageal variceal bleeding continues to be one of the most feared and deadly complications of cirrhosis and portal hypertension, but great progresses have been made in prevention and treatment strategies. Other bleeding sites that are frequently part of end-stage liver disease are similar to clinical manifestations of thrombocytopenia, with gum bleeding and epistaxis being very common but fortunately only rarely a cause of life-threatening bleeding. On the contrary, manifestations of coagulation factor deficiencies like soft tissue bleeding and hemartrosis are rare in patients with cirrhosis. As far as thrombotic complications are concerned, portal vein thrombosis is the most common event in patients with cirrhosis, but venous thromboembolism is not infrequent, and results in important morbidity and mortality in patients with cirrhosis, especially those with decompensated disease. Future studies and the more widespread use of point-of-care tests in evaluating hemostasis will aid the clinician in decision making when facing the patient with bleeding or with thrombotic complications, with both ends of a continuum being potentially fatal.

• Bleeding
• Hemorrhage
• Thromboembolism
• Portal vein thrombosis
• Coagulation
• Cirrhosis