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DOI: 10.1055/s-0041-1739158
Missed Gastroduodenal Hemorrhage: Breaking the Rules of Diagnostic Imaging
Case Presentation
A 66-year-old woman presented with abdominal pain to an outside hospital. She was afebrile but had leukocytosis (14.2 × 109/L). During her workup, she was found to have cholelithiasis and choledocholithiasis on magnetic resonance cholangiopancreatography. During her hospital stay, she underwent laparoscopic cholecystectomy which, for reasons unclear, required conversion to an open procedure. Following surgery, due to suspicion for biliary duct injury, a percutaneous transhepatic cholangiography was performed which demonstrated occlusion of the extrahepatic biliary duct. There was also a high clinical suspicion for vascular injury or occlusion at the level of the porta hepatis as well, confirmed by computed tomographic (CT) scan. A percutaneous biliary drain and right-side peritoneal drain were placed urgently, and she was transferred to the authors' institution for advanced level of care.
Upon arrival, she was intubated and sedated. She immediately underwent surgery and was found to have no blood flow through the right hepatic artery or right portal vein, as well as a transected common hepatic duct. A right hepatectomy with bilioenteric anastomosis and placement of a portal vein saphenous vein conduit was performed with continuation of her antibiotic regimen. Her immediate postoperative course was complicated, but she continued to slowly improve clinically.
On postoperative day (POD) 5, interventional radiology (IR) was consulted because of concerns for occlusion of her portal vein conduit, due to decreased velocity on ultrasound. She underwent mage-guided portal reconstruction with a 14 × 40 mm bare metal stent placed across the entire portal vein conduit; excellent portal venous blood flow was noted following the procedure ([Fig. 1]). Postprocedure, she remained intubated and was admitted to the intensive care unit (ICU) but again demonstrated a slow but steady recovery.
On POD 9, she was found to be anemic to 8 g/dL, down from her baseline value of 9.8 g/dL. She was started on intravenous iron and erythropoietin. Two days later (POD 11), the patient was found to be tachycardic with a heart rate in the 100s with black tarry stools. An esophagogastroduodenoscopy (EGD) was performed which showed ulcerative esophagitis and some gastritis, the former of which was thought to be due to a previously malpositioned nasogastric tube. In addition to her esophagitis and gastritis, hemobilia was suspected due to a clot at the level of the papilla noted during EGD. During endoscopy, no active bleeding was noted. Flexible sigmoidoscopy performed at the same time demonstrated only melanotic stool with no active bleeding.
Over the 5 subsequent days, the patient received seven units of packed red blood cells and six units of fresh frozen plasma. Due to concerns of continued gastrointestinal bleed (GIB), a repeat EGD was performed on POD 16. Endoscopy at that time demonstrated active bright red blood exiting the papilla where a biliary stent was located. The biliary stent was removed endoscopically, and IR was consulted for angiography to evaluate for a source of hemobilia.
Angiography on POD 16 showed no evidence of active contrast extravasation from the celiac, gastroduodenal, common hepatic, superior mesenteric, or right inferior phrenic arteries. No underlying source for arterial bleeding was noted. She remained stable for 5 subsequent days; however, on POD 21 her hemoglobin began to down trend from 10 to 9.3 g/dL with an increased lactate to 1.9 mmol/L.
The morning of POD 22 the patient presented with acute hemorrhagic shock. Given the high likelihood of GIB, emergent EGD and emergent angiogram were requested. The patient was too unstable to be transferred to undergo a CT scan. She was taken emergently to the operating room for potential exploratory laparotomy. Prior to laparotomy, an EGD was performed in the operating room which revealed fresh blood in the second portion of the duodenum, but due to the amount of blood, no specific source of hemorrhage was identified. The working diagnosis, given the prior hemobilia, was recurrent hemobilia with blood in the duodenum coming from the papilla. The IR service placed two large bore central venous catheters and a radial arterial line while endoscopy was being performed. Upon transferring the blood product and vasopressors to the newly placed catheters, the patient stabilized, and the decision was made to transfer her to IR for emergent angiography and embolization.
While awaiting transfer to the IR suite, the prior angiography from 6 days previously was reviewed. Close scrutiny of the hepatic arterial angiography was performed due to the recurrent EGD findings of hemobilia. During review of the angiography, it was determined that an angiographic “pseudovein sign” was present in a segment IV branch ([Fig. 2a–c]). In addition, there was also an irregularity noted in the left hepatic artery that initially was thought to be a surgical anastomosis but was later deemed to be a dissection ([Fig. 2d]). After reviewing the angiography and transfer to the angiography suite, she underwent celiac and hepatic artery angiography.
During angiography, the initial celiac injection demonstrated marked narrowing of all celiac vessels attributed to vasoconstriction secondary to hypotension and the use of multiple vasodilators ([Fig. 3a]). Intra-arterial nitroglycerin was given to facilitate advancement of the catheter to the hepatic artery. Hepatic injection showed a markedly narrowed left hepatic artery at the site of the stenosis noted on the prior angiography. This narrowing was critical and much worse than previously noted ([Fig. 3b]).
Due to the pseudovein finding noted on the prior angiography, catheterization of the segment IV arterial supply was aggressively pursued. Due to the critical proximal stenosis in the left hepatic artery, proximal angiography was nondiagnostic because of the lack of adequate contrast in the intrahepatic arterial branches. It was also very difficult to advance a wire through the narrowed proximal left hepatic artery, and a significant amount of time was spent in obtaining diagnostic images of the previously noted distribution of the pseudovein sign ([Fig. 3c]). Eventually, active contrast extravasation in the left hepatic artery distribution was ruled out.
It was decided by the IR and transplant surgery services that stenting of the proximal left hepatic artery, now deemed to likely represent an evolving arterial dissection, was indicated to prevent ischemic injury to the remaining liver. Due to multiple logistical problems as well as unfavorable anatomy, it took a prolonged time for eventual delivery of a monorail 4-mm bare metal coronary stent, which resulted in good flow through the hepatic artery ([Fig. 4]). Due in part to the continued tenuous hemodynamic status of the patient (she was likely in disseminated intravascular coagulopathy as evidenced by uncontrollable bleeding from her nose and around her tracheostomy tube), empiric embolization of the gastroduodenal artery (GDA) was decided upon.
Gastroduodenal artery angiography demonstrated very brisk contrast extravasation from the proximal GDA, possibly arising from the superior pancreaticoduodenal arteries ([Fig. 5a]). Embolization was performed to stasis with a combination of steel and platinum coils ([Fig. 5b]). A final angiography from the superior mesenteric artery was performed to preclude contrast extravasation from the inferior pancreaticoduodenal arteries. The patient was returned to the ICU in critical but stable condition.
After a long and complicated postprocedural period, the patient died on POD 27.
Publication History
Article published online:
24 November 2021
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