Surgical Treatment of Pancreaticoduodenal Artery Aneurysm Due to Median Arcuate Ligament Syndrome for Which Intraoperative Doppler Ultrasonography Was BeneficialA Case Report.

To the Editor:

Although the first case of a pancreaticoduodenal artery aneurysm (PDAA) was reported by Ferguson[1] in 1895, most of the publications since then have been case reports. Pancreaticoduodenal artery aneurysms are rare and account for 2% of all visceral aneurysms.[2] Almost half of all PDAAs are associated with celiac axis stenosis (CAS)[2] and median arcuate ligament (MAL) compression, which creates a “hooked” appearance that is characteristic of MAL syndrome (MALS), noted in 10% to 30% of such cases.[3] In these cases, division and resection of the PDAA during surgery can cause ischemic complications, including anastomotic dehiscence, abscess formation, and liver failure. Hence, a gastroduodenal artery (GDA) clamping test is mandatory for evaluating hepatic arterial blood flow before resection. Poor hepatic arterial perfusion during the GDA clamping necessitates MAL release to restore the arterial blood flow. To the best of our knowledge, few reports have described quantitative criteria for hepatic arterial blood flow restoration. Herein, we report a case of a PDAA with MALS, surgically treated after quantitatively evaluating the intrahepatic arterial blood flow using intraoperative Doppler ultrasonography.

CASE REPORT

A 79-year-old Japanese man was referred to us with anemia. Colonoscopy revealed an ascending-colon cancer (type 2, stage IIIB). Moreover, a sagittal maximum-intensity projection computed tomography angiogram and 3-dimensional volume–rendered imaging identified a PDAA (33 mm in diameter) with MALS (Figs. 1A, B). Resections of the PDAA and the ascending-colon cancer were planned. The GDA clamping test was performed by measuring the intrahepatic arterial blood flow using Doppler ultrasonography before resection (Fig. 1C). The peak systolic velocity of the intrahepatic arterial flow was 33.2 cm/s before resection; it decreased to 27.9 cm/s after the GDA clamping, suggesting the need for MAL release to minimize the risk of ischemic complications. After the MAL release, the peak systolic velocity of the intrahepatic arterial blood flow, while continuing GDA clamping, increased to 34.7 cm/s, and the resistive index (RI) was maintained within the appropriate range at 0.56. Therefore, revascularization or reconstruction of the common hepatic artery was deemed unnecessary, and the PDAA and ileocecal resections were performed. The postoperative course was uneventful. Postoperative abdominal computed tomography at 1 year 9 months showed no recurrence of the PDAA or CAS.

FIGURE 1

Three-dimensional volume–rendered images and sagittal maximum-intensity projection computed tomography angiogram. A, The PDAA (33 mm in diameter, arrow head). B, Acute angulation and narrowing of the proximal celiac axis has caused poststenotic dilatation, creating a “hooked” appearance (arrow). C, After the MAL was released, the peak systolic velocity of intrahepatic blood flow was restored to 34.7 cm/s during the GDA clamping. The RI was also restored to 0.56. CHA indicates common hepatic artery; PDA, pancreaticoduodenal artery.

DISCUSSION

Pancreaticoduodenal artery aneurysms are usually asymptomatic, and a ruptured aneurysm is often fatal if untreated. The aneurysmal size is unrelated to the risk of rupture, so all PDAAs should be treated, regardless of size.[3]

Two treatment approaches, surgical resection or embolization, are currently followed. Embolization is less invasive but may cause intraoperative aneurysmal rupture or ischemic injury due to the absence of major collateral vessels.[4] In addition, without CAS repair, new aneurysms or recurrence may occur. At present, no consensus exists in the literature on the management of PDAAs with MALS. Importantly, although surgical resection of PDAAs is curative, they involve the risk of life-threatening ischemic complications.[5,6]

Doppler ultrasonography can be used to assess the blood flow qualitatively and quantitatively during liver transplantation.[7,8] The normal Doppler waveform of a hepatic artery shows a rapid systolic upstroke after continuous diastolic flow. Acceleration time and RI can serve as indicators of hepatic arterial blood flow. Acceleration time, the time from the end of diastole to the first systolic peak, should be less than 80 ms; RI, calculated as (peak systolic velocity – end diastolic velocity)/peak systolic velocity, should be between 0.5 and 0.7.[7] A tardus-parvus waveform pattern, with an acceleration time greater than 80 ms and a RI less than 0.5, indicates insufficient arterial flow due to hepatic artery stenosis during liver transplantation.[8] In our case, although the acceleration time was not measured during the clamping test, the peak and mean velocities and RI were decreased reproducibly in comparison with the baseline levels.

A reproducible decrease in hepatic arterial blood flow during the GDA clamping test necessitates MAL release. Moreover, recovery to baseline blood flow levels after MAL release eliminates the need for additional hepatic artery reconstruction. Because PDAAs with MALS are rare, the criteria may appropriately be determined using liver transplant surgery data. Large studies on hepatic artery assessment using Doppler ultrasonography are needed to define the threshold for MAL release or hepatic artery reconstruction during the resection of PDAAs with MALS.

CONCLUSIONS

The intraoperative quantitative evaluation of intrahepatic arterial blood flow using Doppler ultrasonography enabled successful resection of the PDAA because of MALS.