BACKGROUND
Although arterial hemorrhage after pancreaticoduodenectomy (PD) is not frequent, it is fatal. Arterial hemorrhage is caused by pseudoaneurysm rupture, and the gastroduodenal artery stump and hepatic artery (HA) are frequent culprit vessels. Diagnostic procedures and imaging modalities are associated with certain difficulties. Simultaneous accomplishment of complete hemostasis and HA flow preservation is difficult after PD. Although complete hemostasis may be obtained by endovascular treatment (EVT) or surgery, liver infarction caused by hepatic ischemia and/or liver abscesses caused by biliary ischemia may occur. We herein discuss therapeutic options for fatal arterial hemorrhage after PD.
AIM
To present our data here along with a discussion of therapeutic strategies for fatal arterial hemorrhage after PD.
METHODS
We retrospectively investigated 16 patients who developed arterial hemorrhage after PD. The patients’ clinical characteristics, diagnostic procedures, actual treatments [transcatheter arterial embolization (TAE), stent-graft placement, or surgery], clinical courses, and outcomes were evaluated.
RESULTS
The frequency of arterial hemorrhage after PD was 5.5%. Pancreatic leakage was observed in 12 patients. The onset of hemorrhage occurred at a median of 18 d after PD. Sentinel bleeding was observed in five patients. The initial EVT procedures were stent-graft placement in seven patients, TAE in six patients, and combined therapy in two patients. The rate of technical success of the initial EVT was 75.0%, and additional EVTs were performed in four patients. Surgical approaches including arterioportal shunting were performed in eight patients. Liver infarction was observed in two patients after TAE. Two patients showed a poor outcome even after successful EVT. These four patients with poor clinical courses and outcomes had a poor clinical condition before EVT. Fourteen patients were successfully treated.
CONCLUSION
Transcatheter placement of a covered stent may be useful for simultaneous accomplishment of complete hemostasis and HA flow preservation.
Background: Gastric artery aneurysms are rarely caused by segmental arterial mediolysis (SAM), a condition that often involves multiple vessels. The clinical course of SAM after vessel rupture may vary depending on the involved vessels. For example, the "double-rupture phenomenon" observed following the rupture of the splenic artery aneurysm manifests as a biphasic and relatively slow clinical course. Even in cases of rupture of gastric artery aneurysm, the double-rupture phenomenon has only been reported in two cases so far. However, the rupture was not caused by SAM in either case. Herein, we present the apparent first case of a right gastric artery (RGA) aneurysm rupture caused by SAM that presented with a biphasic clinical course, possibly due to the double-rupture phenomenon. Case presentation: A 54-year-old woman was transferred to the emergency department with severe abdominal pain and a cold sweat for a duration of 3 h. She had developed mild abdominal pain and nausea 3 days earlier. Her vital signs were stable. Physical examination revealed tenderness in the epigastric area. Abdominal contrastenhanced computed tomography revealed an RGA aneurysm with contrast media extravasation. A diagnosis of hemoperitoneum following a ruptured RGA aneurysm was made, and the patient underwent angiography. However, this modality did not reveal any extravasation from the RGA due to an interruption in the peripheral branch of the artery. Nevertheless, to prevent major bleeding, we performed coil embolization at the point of interruption in the RGA, which we suspected to be a ruptured aneurysm. A distal gastrectomy with Roux-en-Y reconstruction for aneurysm resection was performed the following day. There were no postoperative complications, and the patient was discharged 17 days after surgery. Histologically, the RGA demonstrated multiple vacuoles in the medial muscle layer, which were characteristic of SAM. Conclusions: An RGA aneurysm rupture should be considered a differential diagnosis in patients presenting with hemoperitoneum with a slow or biphasic clinical course.
Highlights
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