Related Experiment Video
Updated: Sep 21, 2025
Endoscopic Injection Sclerotherapy Assisted by Cyanoacrylate and Clips for Gastroesophageal Varices
Published on: June 13, 2025
Clinical outcomes of gastrointestinal bleeding management during anticoagulation therapy
Ho-Jun Jang1, Dongyoung Lee2, Tae-Hoon Kim3
1Division of Cardiology, Sejong General Hospital, Bucheon, Republic of Korea.
Insights
Managing gastrointestinal bleeding during oral anticoagulation requires careful strategy. Individualized risk assessment is key to preventing serious thromboembolic or rebleeding events in patients on anticoagulation therapy.
Area of Science:
- Cardiology
- Gastroenterology
- Pharmacology
Background:
- Acute gastrointestinal (GI) bleeding is a known complication of oral anticoagulation (OAC) therapy.
- Cessation of OAC can lead to fatal stroke or systemic embolization in high-risk patients.
- Optimal OAC cessation strategies following GI bleeding are not well-defined.
Purpose of the Study:
- To investigate appropriate anticoagulation cessation strategies for patients experiencing GI bleeding during OAC therapy.
- To compare thromboembolic and rebleeding event rates between OAC continuation and discontinuation groups.
Main Methods:
- Single-center retrospective cohort analysis (2010-2018).
- Inclusion criteria: atrial fibrillation, OAC therapy, and GI bleeding.
- Patients categorized into OAC continuation or discontinuation groups for 1-year follow-up.
Main Results:
- 146 patients analyzed; 54 in continuation, 92 in discontinuation.
- No significant difference in major embolic stroke rates (3.7% vs. 2.2%) or rebleeding events (7.4% vs. 5.4%) between groups.
- Glasgow-Blatchford score predicted rebleeding; high CHA₂DS₂-VASc score trended towards thromboembolic events.
Conclusions:
- No single risk factor or cessation strategy was definitively linked to adverse events post-GI bleed.
- Individualized risk stratification is crucial for managing thrombotic and rebleeding risks.
- Tailoring OAC management based on patient-specific risk scores is recommended.
Background:
Acute gastrointestinal (GI) bleeding is not an uncommon complication of oral anticoagulation (OAC) therapy that requires medication cessation. However, drug cessation may cause fatal stroke or systemic embolization in patients at high thromboembolic risk. Here we sought to find an appropriate anticoagulation cessation strategy in cases of GI bleeding during OAC therapy.
Methods:
This single-center retrospective cohort analysis was performed between 2010 and 2018. Patients were enrolled if the following three consecutive conditions were met: 1) electrocardiography electrocardiography-proven atrial fibrillation; 2) OAC therapy; and 3) GI bleeding. We divided the drug cessation strategy into the continuation and discontinuation groups. During 1-year follow-up, the rates of major thromboembolic and rebleeding events were calculated.
Results:
One hundred and forty-six patients (continuation [n = 54] vs. discontinuation [n = 92] group) were enrolled. Patients in the discontinuation group were more likely to be older (69.8 ± 9.0 yrs vs. 74.9 ± 8.9 yrs, p = 0.001), while patients in the continuation group were more likely to have undergone cardiac valve surgery (51.9% vs. 20.7%, p<0.001). The presence of a mechanical mitral valve was a determinant of continuation strategy (38.9% vs. 7.5%, p<0.001). However, the mean CHA₂DS₂-VASc (3.4±1.3 vs. 4.1±1.6, p = 0.010) and Glasgow-Blatchford (8.0±2.4 vs. 8.9±2.5, p = 0.037) scores were higher in the discontinuation group. Two major embolic strokes occurred in each group (3.7% vs. 2.2%, p = 0.585). Four of 54 (7.4%) and five of 92 (5.4%) patients had rebleeding events during follow-up (p = 0.632). One embolic event in the continuation group and one rebleeding event in the discontinuation group were fatal. The Glasgow-Blatchford score was a predictor of 1-year rebleeding events (odds ratio [OR], 1.36; 95% confidence interval [CI], 0.68-2.20; p = 0.028). The high CHA₂DS₂-VASc score showed a strong trend (OR, 1.71; 95% CI, 0.92-3.20; p = 0.089) in 1-year thromboembolic events.
Conclusion:
No single risk factor or drug cessation strategy was attributed to adverse clinical events after GI bleeding. The risk of future thrombotic or rebleeding events should be individualized and controlled for based on a pre-existing stratification system.
Related Concept Videos
01:28Esophageal Varices-II: Clinical Features and Management
In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol...
01:30Venous Thrombosis IV: Nursing Management
01:29Venous Thrombosis III: Interprofessional Care
01:30Anticoagulant Drugs: Low-Molecular-Weight Heparins
01:18Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
01:23Gastritis III: Clinical Manifestations and Management
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...