Surgical case reports · 2026
Planned Distal Pancreatectomy and Splenectomy for Pancreatic Tail Necrosis and Splenic Infarction after Embolization for Gastric Ulcer-Induced Splenic Artery Perforation: A Case Report.
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Saito Yasutaka, Masiko Kazuki, Ueda Taichiro, Hara Yoshiaki
Аннотация
INTRODUCTION: Splenic artery perforation secondary to gastric ulcer is a rare but life-threatening cause of upper gastrointestinal bleeding. Splenic artery embolization (SAE) can provide rapid hemorrhage control, but delayed ischemic complications involving the pancreatic tail and spleen are uncommon.
CASE PRESENTATION: A woman in her 70s presented with hematemesis and profound hemorrhagic shock. Contrast-enhanced CT showed active extravasation from the splenic artery adjacent to the posterior gastric wall. During emergency SAE, coils were deployed across the bleeding point, but persistent extravasation required additional embolization with a 1:2 mixture of N-butyl-2-cyanoacrylate (NBCA) and lipiodol. Final angiography confirmed hemostasis with preservation of the dorsal and great pancreatic arteries. CT on hospital day 2 showed no apparent pancreatic ischemic change. On day 11, newly developed hypoattenuating areas involving the pancreatic tail and part of the spleen were detected, suggestive of ischemic changes. The patient had no abdominal pain or overt clinical deterioration. Laboratory abnormalities that had improved by day 8 showed a secondary increase on day 11, with a white blood cell count of 12200/μL, C-reactive protein level of 3.90 mg/dL, and serum amylase level of 456 U/L. Planned distal pancreatectomy and splenectomy were selected after individualized assessment of the pancreatic and splenic ischemic changes, together with a residual splenic hilar aneurysmal lesion and suspected posterior gastric wall penetration. Pathological examination confirmed pancreatic necrosis and splenic infarction. No postoperative pancreatic fistula or other major postoperative complication occurred, and the patient was discharged on hospital day 38 after rehabilitation.
CONCLUSIONS: NBCA-assisted SAE can achieve rapid hemostasis in life-threatening splenic arterial bleeding, but post-embolization surveillance remains important. This case illustrates that management of post-SAE ischemic changes should be individualized and that planned surgery in a clinically stable patient should be based on the overall clinical and anatomical context.
CASE PRESENTATION: A woman in her 70s presented with hematemesis and profound hemorrhagic shock. Contrast-enhanced CT showed active extravasation from the splenic artery adjacent to the posterior gastric wall. During emergency SAE, coils were deployed across the bleeding point, but persistent extravasation required additional embolization with a 1:2 mixture of N-butyl-2-cyanoacrylate (NBCA) and lipiodol. Final angiography confirmed hemostasis with preservation of the dorsal and great pancreatic arteries. CT on hospital day 2 showed no apparent pancreatic ischemic change. On day 11, newly developed hypoattenuating areas involving the pancreatic tail and part of the spleen were detected, suggestive of ischemic changes. The patient had no abdominal pain or overt clinical deterioration. Laboratory abnormalities that had improved by day 8 showed a secondary increase on day 11, with a white blood cell count of 12200/μL, C-reactive protein level of 3.90 mg/dL, and serum amylase level of 456 U/L. Planned distal pancreatectomy and splenectomy were selected after individualized assessment of the pancreatic and splenic ischemic changes, together with a residual splenic hilar aneurysmal lesion and suspected posterior gastric wall penetration. Pathological examination confirmed pancreatic necrosis and splenic infarction. No postoperative pancreatic fistula or other major postoperative complication occurred, and the patient was discharged on hospital day 38 after rehabilitation.
CONCLUSIONS: NBCA-assisted SAE can achieve rapid hemostasis in life-threatening splenic arterial bleeding, but post-embolization surveillance remains important. This case illustrates that management of post-SAE ischemic changes should be individualized and that planned surgery in a clinically stable patient should be based on the overall clinical and anatomical context.