A 51-year-old healthy female without significant past medical history presented to the emergency department with severe nonradiating abdominal pain that began without an inciting event. The pain was mainly located in the epigastric region. The pain was described as sharp and was associated with nausea; multiple episodes of nonbloody, nonbilious emesis; chills; and a near syncopal episode. There were no specific alleviating or exacerbating factors, and she never had similar symptoms in the past. She denied any fever, dysuria, history of heartburn, peptic/duodenal ulcer disease, heavy nonsteroidal anti-inflammatory drugs (NSAID) use, recent illnesses, recent ill contacts, or recent travel. She denied any significant surgical history. She is a former heavy smoker and reported current moderate alcohol use and a recent increase in her stress level. The patient denied a prior history of EGD or colonoscopy. Family history is significant for coronary artery disease in both parents.
In the emergency department, she was found to be hypotensive with a blood pressure of 64/48 mmHg and a heart rate of 71 bpm. Her oxygen saturation was 100% on room air. Physical exam revealed a diffusely tender abdomen. Lab tests were significant for a hemoglobin of 9.1 g/dL and a white blood count of 14.4 k/muL. Subsequently, 2 large-bore intravenous (IV) catheters were inserted and a blood type and screen were ordered. IV fluids were started along with pain and nausea control medications.
A contrast-enhanced CT scan of the abdomen and pelvis revealed a large retroperitoneal hematoma with a lobulated focus of active contrast extravasation interposed between the pancreatic head and the duodenum (Figure 1). The bleeding was localized to the retroperitoneum itself and did not involve nearby retroperitoneal organs such as the pancreas, kidneys, or duodenum; however, these organs did show displacement by the hematoma. Several nearby vessels were identified as the potential source of bleeding including the distal gastroduodenal artery as well as several prominent superior and inferior pancreaticoduodenal (PDA) arteries extending from the gastroduodenal and superior mesenteric arteries, respectively. Finally, a high-grade proximal celiac artery stenosis was noted consistent with median arcuate ligament compression (Figure 2). Interventional radiology (IR) and general surgery were consulted, and a mesenteric angiogram was emergently performed to localize the bleeding for potential embolization.
Mesenteric angiography confirmed median arcuate ligament compression that was well compensated through brisk extensive collateral flow from the SMA via the pancreaticoduodenal arcade (Figure 3). Embolization of an inferior pancreaticoduodenal (PDA) branch was performed with detachable 0.018-inch coils given active extravasation. Further interrogation showed the abnormal aneurysmal pancreaticoduodenal vessel, but the structure was unable to be reached given only a small network of feeding arteries measuring 1 mm or less (Figure 4). No further bleeding was identified. Although the patient's condition immediately improved following embolization, there was still potential for further hemorrhage given the untreated aneurysm. Since this, after hours, treatment was prolonged with both resuscitation and procedure time, and the patient improved clinically; she was transferred to the ICU for observation and further workup. An arterial sheath was left in place for blood pressure monitoring and potential subsequent access given an incomplete interrogation of the complex anatomy. Initial management included intravenous proton pump inhibitor, placement of the nasogastric tube, and order for the serial blood counts, and a gastroenterology consult was obtained.
Later that day, the patient complained of continued epigastric abdominal pain and nausea, but vital signs remained stable. A follow-up CT scan with contrast was ordered and showed the hematoma was slightly larger containing a new bilobed 2 cm saccular area of circulating contrast. This was defined as a residual saccular pseudoaneurysm, rather than a true aneurysm, given new morphology when compared to the prior scan, and likely contained by the hematoma within the tight retroperitoneal tissues. The nearby fusiform aneurysm was not seen, presumably decompressed from rupture. The patient also required a blood transfusion given slowly dropping hemoglobin values. Although vital signs were stable, angiography was again performed given her laboratory deterioration and CT findings. The new pseudoaneurysm was identified, but unfortunately the feeding vessel remained occult after integration of multiple branches including several branches of the inferior pancreaticoduodenal artery. Given the procedure time, contrast dose, and continued relative stability of the patient, the procedure was terminated.
The vascular surgery team decided against celiac release in the acute setting given the risks of the surgery and current blood loss but agreed that a median arcuate ligament release would likely be needed as an outpatient. The patient remained stable, but there was continued suspicion for a slow hemorrhage from the ruptured aneurysm. A third mesenteric angiogram was again performed on day 2 but this time with angiography of the celiac artery and gastroduodenal artery (GDA) via the high-grade celiac artery stenosis. Using digital subtraction angiography (DSA), a prominent superior PDA branch supplying the aneurysm was identified and treated with coil embolization (Figures 5(a) and 5(b)). Access from the celiac was removed, and SMA angiography demonstrated persistence of the aneurysm. Given the complexity of the PDA anatomy, cone beam CT angiography (GE Innova 540) with subsequent 3D reconstruction was performed. The 2D maximum intensity projection (MIP) images not only clearly demonstrated the PSA but also showed a second culprit posterior inferior PDA supplying the pseudoaneurysm. The gantry angle was optimized from the 3D volume rendering (Figure 6), and image overlay of live fluoroscopy allowed for quick vessel selection with the microcatheter/microwire. After verification with DSA, the vessel was treated with coil embolization (Figures 7(a) and 7(b)) thrombosing the PSA.
The following day, she reported feeling well with less pain and nausea. Her hemoglobin and vital signs were stable. NG was removed, and her diet was advanced. The remainder of her hospital stay was unremarkable other than hypertension treated with lisinopril, hydrochlorothiazide, and metoprolol to aid in avoiding further rebleeding events.