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Updated: May 28, 2026

Laparoscopic Splenectomy with Pericardial Devascularization for Hypersplenism and Esophageal Variceal Hemorrhage Due to Portal Hypertension
Published on: November 15, 2024
Endoscopic Hemostasis as a Bridge to Surgical Portal Decompression in Children with Portal Hypertensive Bleeding: A
Jianji Xu1, Jinshan Zhang1, Chihuan Kong1
1Department of General Surgery, Capital Institute of Pediatrics, Capital Medical University, Beijing 100020, China.
Insights
A staged approach using endoscopic hemostasis followed by surgery effectively manages pediatric portal hypertension bleeding. Early Rex shunt dysfunction was noted in very young children, requiring further study.
Area of Science:
- Pediatric Gastroenterology
- Surgical Gastroenterology
- Vascular Surgery
Background:
- Portal hypertension is a primary cause of esophagogastric variceal bleeding in children.
- Endoscopic therapy achieves acute hemostasis but doesn't address underlying physiology, often necessitating surgical decompression.
- Limited evidence exists on staged endoscopic-surgical management for pediatric portal hypertension.
Purpose of the Study:
- To evaluate clinical outcomes of children with portal hypertensive bleeding.
- To assess endoscopic hemostasis as a bridge to definitive portal decompression surgery.
- To analyze rebleeding, shunt patency, and survival rates in this pediatric cohort.
Main Methods:
- Retrospective cohort study of 12 children with portal hypertension-related variceal bleeding.
- All patients received endoscopic hemostasis followed by surgical portal decompression when feasible.
- Outcomes analyzed included hemostasis success, rebleeding, shunt patency, survival, and age-related Rex shunt dysfunction.
Main Results:
- Endoscopic hemostasis succeeded in all patients with no early rebleeding.
- Ten patients underwent surgery within 7 days (8 Rex shunt, 2 splenorenal shunt).
- Median follow-up of 18 months revealed early Rex shunt dysfunction in 25% of patients younger than 3 years; rebleeding and mortality were linked to shunt dysfunction.
Conclusions:
- A staged endoscopic-surgical strategy is feasible for stabilizing pediatric portal hypertensive bleeding and facilitating timely decompression.
- Early Rex shunt dysfunction may be more prevalent in very young children (<3 years), warranting cautious interpretation and further research.
- This approach offers a viable pathway for managing complex pediatric cases, though larger studies are needed.
Abstract:
Background: Portal hypertension is a major cause of esophagogastric variceal bleeding in children. Endoscopic therapy is widely used for acute hemostasis; however, it primarily controls the bleeding episode rather than the underlying portal hypertensive physiology, and definitive management often requires surgical portal decompression. Evidence regarding the outcomes of a staged endoscopic-surgical management strategy in pediatric patients remains limited. This study aimed to evaluate the clinical outcomes of children with portal hypertensive bleeding managed with endoscopic hemostasis as a bridging therapy followed by definitive portal decompression surgery. Methods: We conducted a retrospective consecutive cohort study including 12 children presenting with portal hypertension-related variceal bleeding at our tertiary pediatric center between January 2021 and December 2024. All patients underwent endoscopic hemostasis, followed by evaluation for portal decompression surgery when anatomically feasible. Clinical outcomes including hemostasis success, rebleeding, shunt patency, and survival were analyzed. An age-stratified exploratory analysis was performed to examine the association with early dysfunction after Rex shunt reconstruction. Results: Endoscopic hemostasis was successfully achieved in all patients, with no early rebleeding prior to surgery. Ten patients underwent portal decompression surgery within 7 days (Rex shunt, n = 8; splenorenal shunt, n = 2). During a median follow-up of 18 months, early Rex shunt dysfunction (<3 months) was observed in 2 of 8 patients (25%), both of whom were younger than 3 years, whereas no dysfunction was observed in older children. Given the small sample size, this observation should be interpreted descriptively. Rebleeding and mortality occurred exclusively in association with shunt dysfunction. Conclusions: A staged endoscopic-surgical strategy appears feasible for stabilizing children with acute portal hypertensive bleeding and enabling timely definitive portal decompression. In this small cohort (n = 12), an age-related signal in early Rex shunt dysfunction was observed in very young children; however, this finding should be interpreted cautiously and requires further validation in larger studies.
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