Massive bleeding from a Bricker ileal conduit during FOLFIRINOX therapy in noncirrhotic portal hypertension: suspected oxaliplatin-associated sinusoidal injury and presumed irinotecan-associated conduit mucositis: a case report

BACKGROUND: Bleeding from an ileal conduit after radical cystectomy is uncommon and is usually attributed to tumor recurrence, infection, stones, or local stomal trauma. Portal hypertensive stomal varices are rare. FOLFIRINOX adds further diagnostic complexity because oxaliplatin may cause sinusoidal endothelial injury and noncirrhotic portal hypertension, whereas irinotecan may damage gastrointestinal mucosa. We report a case of massive hemorrhage from a long-functioning Bricker ileal conduit during FOLFIRINOX therapy. CASE PRESENTATION: A 72-year-old man with prior radical cystoprostatectomy with Bricker diversion in 2022, robot-assisted left adrenalectomy in 2023, and pancreatic head adenocarcinoma treated with FOLFIRINOX was admitted in February 2026 because of sudden gross hematuria that rapidly filled the urostomy bag with blood and clot. He had received two FOLFIRINOX cycles. With a height of 170 cm and weight of 70 kg, body-surface area was 1.82 m² by the Mosteller formula. Using the standard FOLFIRINOX oxaliplatin dose of 85 mg/m², the reconstructed cumulative oxaliplatin exposure was approximately 170 mg/m², corresponding to about 310 mg in total. Bleeding began 8 days after the most recent irinotecan-containing cycle. Contrast-enhanced computed tomography showed periportal tumor-related changes with a biliary stent, variceal collaterals adjacent to the conduit, and circumferential thickening of the conduit wall, whereas the upper urinary tracts were nondilated and there was no radiologic evidence of recurrent urothelial carcinoma. Looposcopy demonstrated diffusely inflamed and friable conduit mucosa, but biopsy was not performed. Doppler ultrasonography demonstrated portal vein dilatation with preserved hepatopetal flow and no imaging features of cirrhosis. Platelet counts remained within the reference range, and retrospective review of restaging computed tomography showed no interval splenomegaly; the craniocaudal splenic length was approximately 11 cm and unchanged. Urine culture grew extended-spectrum beta-lactamase-producing Escherichia coli and Enterococcus faecalis, but inflammatory markers remained low and there were no clinical features of sepsis. The most cautious interpretation was a mixed mechanism: portal hypertensive stomal varices, possibly related to pancreatic venous distortion and/or early oxaliplatin-associated sinusoidal injury, compounded by presumed irinotecan-associated conduit mucositis. Bleeding ceased with supportive, anti-inflammatory, antimicrobial, transfusion, and nonselective beta-blocker therapy. By May 2026, conduit bleeding had not recurred, although the patient remained chronically unwell with poor ECOG performance status because of the underlying pancreatic cancer. CONCLUSIONS: Massive bleeding from a Bricker conduit during FOLFIRINOX therapy may be multifactorial. Early portal-phase imaging and portal venous assessment are essential when hemorrhage is disproportionate to routine urinary tract findings. In the absence of histology, catheter venography, and portal pressure measurement, causal language should remain cautious. If bleeding recurs, management should move beyond local measures and consider venous mapping, targeted embolization or sclerotherapy, portal decompression or venous stenting in suitable anatomy, and surgical undiversion to bilateral cutaneous ureterostomies when durable conduit preservation appears unlikely.