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.