Gastrointestinal bleeding due to rupture of esophageal varices is a major and potentially fatal complication of portal hypertension. Endoscopic band ligation is currently considered the gold-standard treatment. However, rebleeding following ligation remains a serious event, and the factors associated with its occurrence are not yet clearly defined. The objective of this study was to assess the prevalence and identify the predictive factors of recurrent bleeding after endoscopic band ligation of esophageal varices.

A prospective, descriptive, and analytical study was conducted over a one-year period, from December 2023 to December 2024. It included fifty-nine patients with portal hypertension who underwent endoscopic band ligation of esophageal varices.

The collected data included demographic characteristics, etiology of portal hypertension, severity scores of liver disease (Child-Pugh and MELD), endoscopic findings, details of the ligation procedure (number of sessions and bands used), associated treatments, eradication outcomes, recurrence of bleeding, and mortality. All data were obtained from medical records and analyzed using the Jamovi software.

Fifty-nine patients were enrolled in the study. The mean age was 55 ± 15 years (range 18–87 years), with a male-to-female ratio of 1.25. Cirrhosis was the predominant cause of portal hypertension, accounting for 83% of cases (n=49). The main etiologies were viral hepatitis in 24% (n=14), primary biliary cirrhosis in 3% (n=2), autoimmune hepatitis in 2% (n=1), iron overload in 2% (n=1), and nonalcoholic steatohepatitis (NASH) in 2% (n=1). Cryptogenic cirrhosis represented 49% (n=29) of cirrhotic cases. Portal vein thrombosis was found in 15% (n=9), and Budd–Chiari syndrome in 5% (n=3).

The mean follow-up duration was 3.5 ± 3.5 years (range 1–16 years). Secondary prophylaxis was the indication for ligation in 92% of patients (n=54). A history of hematemesis associated with melena was reported in 88% (n=52), while 3% (n=2) had isolated melena. The mean number of previous bleeding episodes was 1.7 ± 1.1 (range 1–7).

Initial endoscopic findings revealed grade III esophageal varices in 85% of patients (n=50) and grade II in 19% (n=11). Portal hypertensive gastropathy was observed in 66% (n=39), and gastric varices were present in 46% (n=27).

A total of 140 ligation sessions were performed. Complete eradication of varices was achieved in 46% of patients (n=27), with a mean of 2.6 sessions per patient. The mean number of bands applied per session was 5 ± 1.9. Four patients achieved eradication after a single session, ten after two sessions, seven after three sessions, six after four sessions, and one patient required six sessions. Beta-blockers were contraindicated in 29% of patients (n=17).

The rebleeding rate was 18% (n=11), occurring after a mean interval of three weeks. Among these patients, 55% were classified as Child-Pugh B, with an average of 2.8 sessions required for eradication. Notably, 63% of patients who experienced rebleeding were not receiving beta-blockers. The mortality rate due to variceal rupture was 8% (n=5).

Statistical analysis did not identify any factor significantly associated with rebleeding after endoscopic band ligation. However, the severity of liver dysfunction, particularly in patients with Child-Pugh B or C scores, appeared to increase the risk of recurrence. Conversely, the use of beta-blockers was significantly associated with a reduced risk of rebleeding. These findings support the combined use of endoscopic band ligation and beta-blocker therapy as an effective strategy for secondary prevention of variceal bleeding.