Effect of ingesting a meal and orthostasis on the regulation of splanchnic and systemic hemodynamics and the responsiveness of cardiovascular α1-adrenoceptors.

Postprandial orthostasis activates mechanisms of cardiovascular homeostasis to maintain normal blood pressure (BP) and adequate blood flow to vital organs. The underlying mechanisms of cardiovascular homeostasis in postprandial orthostasis still require elucidation. Fourteen healthy volunteers were recruited to investigate the effect of an orthostatic challenge (60°-head-up-tilt for 20 min) on splanchnic and systemic hemodynamics before and after ingesting an 800-kcal composite meal. The splanchnic circulation was assessed by ultrasonography of the superior mesenteric and hepatic arteries and portal vein. Systemic hemodynamics were assessed noninvasively by continuous monitoring of BP, heart rate (HR), cardiac output (CO), and the pressor response to an intravenous infusion on increasing doses of phenylephrine, an α1-adrenoceptor agonist. Neurohumoral regulation was assessed by spectral analysis of HR and BP, plasma catecholamine and aldosterone levels and plasma renin activity. Postprandial mesenteric hyperemia was associated with an increase in CO, a decrease in SVR and cardiac vagal tone, and reduction in baroreflex sensitivity with no change in sympathetic tone. Arterial α1-adrenoceptor responsiveness was preserved and reduced in hepatic sinusoids. Postprandial orthostasis was associated with a shift of 500 mL of blood from mesenteric to systemic circulation with preserved sympathetic-mediated vasoconstriction. Meal ingestion provokes cardiovascular hyperdynamism, cardiac vagolysis, and resetting of the baroreflex without activation of the sympathetic nervous system. Meal ingestion also alters α1-adrenoceptor responsiveness in the hepatic sinusoids and participates in the redistribution of blood volume from the mesenteric to the systemic circulation to maintain a normal BP during orthostasis.NEW & NOTEWORTHY A unique integrated investigation on the effect of meal on neurohumoral mechanisms and blood flow redistribution of the mesenteric circulation during orthostasis was investigated. Food ingestion results in cardiovascular hyperdynamism, reduction in cardiac vagal tone, and baroreflex sensitivity and causes a decrease in α1-adrenoceptor responsiveness only in the venous intrahepatic sinusoids. About 500-mL blood shifts from the mesenteric to the systemic circulation during orthostasis. Accordingly, the orthostatic homeostatic mechanisms are better understood.

An Uncommon Variant of Nutcracker Syndrome Secondary to Left Renal Vein Compression Between the Right Renal Artery and The Proper Hepatic Artery.

Nutcracker syndrome refers to the compression of the left renal vein between the abdominal aorta and the superior mesenteric artery. The subsequent venous congestion of the left kidney, when symptomatic, could be associated with left flank pain, hematuria, varicocele, dyspareunia, dysmenorrhea, and proteinuria. Here we describe a 42-year-old female patient with simultaneous Dunbar syndrome and a rare variant of nutcracker syndrome in which the left renal vein (LRV) compression is secondary to the unusual path of the vein between the right renal artery and the proper hepatic artery. For both the nutcracker syndrome and the Dunbar syndrome, open approach by median mini-laparotomic access for transposition of LRV, and resection of the diaphragmatic pillars and arcuate ligament was attempted. During the intervention, due to anatomical issues, the LRV transposition was converted to endovascular stenting of the LRV, moreover the implanted stent was transfixed with an external non-absorbable suture to avoid migration. At the 12 months follow-up the patient was asymptomatic, and the duplex scan confirmed the patency of the celiac trunk without re-stenosis and a correct position of the LRV stent with no proximal or distal migration.

Hepatic Artery Embolization for Postoperative Hemorrhage: Importance of Arterial Collateral Vessels and Portal Venous Impairment.

PURPOSE: To investigate the association between hepatic ischemic complications and hepatic artery (HA) collateral vessels and portal venous (PV) impairment after HA embolization for postoperative hemorrhage. MATERIALS AND METHODS: From October 2003 to November 2019, 42 patients underwent HA embolization for postoperative hemorrhage. HA collateral vessels were classified according to visualization after embolization (grade 1, none; grade 2, 1-4 segmental HA; and grade 3, ≥4 segmental HA). Transhepatic portal vein stent placements were performed in the same session for 5 patients (11.9%) with poor HA collateral vessels (grade 1 or 2) and compromised PV flow (>70% stenosis). Hepatic ischemic complications were analyzed for relevance to HA collateral vessels and PV compromise. RESULTS: After HA embolization, HA flow was found to be preserved (grade 3) through intra- and/or extrahepatic collateral vessels in 23 patients (54.8%), and hepatic complications did not occur regardless of PV flow status (0%). Of the 19 patients (45.2%) with poor HA collateral vessels (grade 1 or 2), segmental hepatic infarction occurred in 2 of 15 patients (13.3%) with preserved PV flow (10 naïve and 5 stented). The remaining 4 patients with poor HA collateral vessels and untreated compromised PV flow experienced multisegmental hepatic infarction (n = 3) or hepatic failure (n = 1) (100%) (P < .005). CONCLUSIONS: After HA embolization, preserved HA flow (≥4 segmental HA) lowered the risk of hepatic complications regardless of the PV flow. Based on these findings, transhepatic PV stent placement seems to be an effective intervention for the prevention of hepatic complications in cases of poor HA collateral vessels and compromised PV flow.

Real-time identification of aberrant left hepatic arterial territories using near-infrared fluorescence with indocyanine green during gastrectomy for gastric cancer.

BACKGROUND: An aberrant left hepatic artery is frequently encountered during upper gastrointestinal surgery, and researchers have yet to propose optimal strategies with which to address this arterial variation. The objective of this study was to determine whether the areas perfused by an aberrant left hepatic artery can be visualized in real-time using near-infrared fluorescence imaging with indocyanine green. METHODS: Patients with gastric adenocarcinoma who underwent minimally invasive radical gastrectomy from May 2018 to August 2019 were enrolled and retrospectively analyzed at a single-center. Patients with an aberrant left hepatic artery and normal preoperative liver function were examined. After the clamping of an aberrant left hepatic artery, indocyanine green was administered via a peripheral intravenous route during surgery. Fluorescence at the liver was visualized under near-infrared fluorescence imaging. RESULTS: In 31 patients with aberrant left hepatic arteries, near-infrared fluorescence imaging was used without adverse events associated with indocyanine green. Six (19%) patients were reported to have an aberrant left hepatic artery upon preoperative CT imaging, while all other instances were detected during surgery. Fluorescence excitation on the liver was, on average, visible after 43 s (range, 25-65). Fluorescence across the entire surface of the liver was noted in 20 (65%) patients in whom the aberrant left hepatic artery could be ligated. Aberrant left hepatic arteries were safely preserved in 10 (32%) patients who showed areas of no or partial fluorescence excitation. Guided by near-infrared fluorescence imaging, ligation of aberrant left hepatic arteries elicited no significant changes in postoperative liver function. CONCLUSION: Near-infrared fluorescence imaging facilitates the identification of aberrant left hepatic arterial territories, guiding decisions on the preservation or ligation of this arterial variation.

Pentafurcated Celiac Trunk.

BACKGROUND: Commonly, but not exclusively, the celiac trunk (CT) trifurcates into the left gastric (LGA), common hepatic (CHA) and splenic (SA) arteries. Additional branches of the CT are scarcely reported in the literature. Less than ten reports were found presenting patterns of pentafurcation of the CT (pCT), all being resulted after anatomic dissections. METHOD: We hereby report such a rare pCT, which was found on the computed tomography angiograms of a 71-year-old female patient. RESULTS: From that pCT were branching off three collateral branches, two ascending and one descending, and two terminal branches. The ascending ones were the left inferior phrenic artery and a secondary hepatogastric trunk, further divided into a replaced left hepatic artery and the left gastric artery. The dorsal pancreatic artery was the descending collateral branch of the pCT. The pCT ended by dividing into the CHA and SA. The CHA reached the anterior side of the portal vein to divide into the gastroduodenal and right hepatic arteries. An accessory right hepatic artery left the superior mesenteric artery (SMA) and ascended posterior to the portal vein. CONCLUSIONS: To the authors' knowledge, the combination of a pCT and a hepatic branch from the SMA, which raises to three the main arteries of the liver, was not reported previously. Additional branches of the CT should be carefully documented by computed tomography prior to surgical or interventional approaches of the aorta in the celiac region.

A Quantitative Digital Subtraction Angiography Technique for Characterizing Reduction in Hepatic Arterial Blood Flow During Transarterial Embolization.

OBJECTIVE: There is no standardized and objective method for determining the optimal treatment endpoint (sub-stasis) during transarterial embolization. The objective of this study was to demonstrate the feasibility of using a quantitative digital subtraction angiography (qDSA) technique to characterize intra-procedural changes in hepatic arterial blood flow velocity in response to transarterial embolization in an in vivo porcine model. MATERIALS AND METHODS: Eight domestic swine underwent bland transarterial embolizations to partial- and sub-stasis angiographic endpoints with intraprocedural DSA acquisitions. Embolized lobes were assessed on histopathology for ischemic damage and tissue embolic particle density. Analysis of target vessels used qDSA and a commercially available color-coded DSA (ccDSA) tool to calculate blood flow velocities and time-to-peak, respectively. RESULTS: Blood flow velocities calculated using qDSA showed a statistically significant difference (p < 0.01) between partial- and sub-stasis endpoints, whereas time-to-peak calculated using ccDSA did not show a significant difference. During the course of embolizations, the average correlation with volume of particles delivered was larger for qDSA (- 0.86) than ccDSA (0.36). There was a statistically smaller mean squared error (p < 0.01) and larger coefficient of determination (p < 0.01) for qDSA compared to ccDSA. On pathology, the degree of embolization as calculated by qDSA had a moderate, positive correlation (p < 0.01) with the tissue embolic particle density of ischemic regions within the embolized lobe. CONCLUSIONS: qDSA was able to quantitatively discriminate angiographic embolization endpoints and, compared to a commercially available ccDSA method, improve intra-procedural characterization of blood flow changes. Additionally, the qDSA endpoints correlated with tissue-level changes.

Hepatic Arterial Blood Flow Modulation in Patients with Hepatocellular Carcinoma: A Pilot Study of the Influence of Intraarterial Norepinephrine Assessed with CT Perfusion.

PURPOSE: This pilot study aims to evaluate the effect of hepatic intraarterial norepinephrine injection in vasculature modulation for hepatocellular carcinoma (HCC) tumors. MATERIALS AND METHODS: This is a single-center prospective study of patients with HCC with proven single-lobe tumors > 3 cm. Eight patients were included, with a mean age of 63 y ± 8. All patients had Barcelona Clinic Liver Cancer stage B HCC and an Eastern Cooperative Oncology Group performance status of 0. Mean tumor size was 6.1 cm ± 1.8; all tumors were hypervascular. Patients underwent CT hepatic perfusion before and after injection of 24 µg of norepinephrine intraarterially (4 µg/mL; total 6 mL injected at a rate of 1 mL/s). Color-coded perfusion maps were used to assess the effects of local therapy on hepatic perfusion values. Tumor-to-liver ratio (TLR) was calculated from the ratio of tumor perfusion to background liver perfusion value. RESULTS: Seven of 8 patents had significant (P = .04) absolute increase in tumor perfusion vs background liver, varying from incremental (-2 mL/min/100 mL) to 290 mL/min/100 mL. There was a nonsignificant increase in TLR from 2.7 ± 1.3 to 2.9 ± 1.4 after norepinephrine injection (P = .8). Mean peak time to maximal increase in tumor perfusion after injection was 6.1 s (range, 4.5-9.1 s). Norepinephrine injection was well tolerated without major adverse events. CONCLUSIONS: Norepinephrine causes increased blood flow toward HCC tumors, but with a corresponding smaller increase in blood flow to noncancerous liver tissue, with no observed systemic side effects.

Application of Hepatic Transit Time and Shear Wave Velocity in Assessing Portal Pressure in Patients with Cirrhotic Portal Hypertension.

The aim of the study described here was to explore the value of hepatic transit time (HTT) and shear wave velocity (SWV) in diagnosing cirrhotic portal hypertension. Fifty-seven patients had undergone esophagogastric varicose vein embolization (group OBS) and 50 healthy controls (group CON) were retrospectively compared with respect to HTT (arterial-hepatic vein [HA-HVTT], portal vein-hepatic vein [PV-HVTT], liver parenchyma-hepatic vein [PA-HVTT]) and SWV to analyze their efficacy in diagnosing cirrhotic portal hypertension. The correlations between SWV/HTT and free portal pressure (FPP) in group OBS were also analyzed. Compared with group CON, group OBS had a shorter HTT and faster SWV. The area under the curve (AUC) of PV-HVTT (0.93) was higher than those of HA-HVTT (0.75) and PA-HVTT (0.64), the AUCs of PV-HVTT (0.93, threshold 7.9 s) and SWV (0.91, threshold 2.0 cm/s) did not statistically differ (z = 0.35, p = 0.73). HTT and FPP in group OBS had a negative correlation. In conclusion, HTT and SWV can be used to diagnose cirrhotic portal hypertension without difference in diagnostic efficacy, and HTT is more meaningful for assessing the changes in portal pressure.

Hyperoxia in portal vein causes enhanced vasoconstriction in arterial vascular bed.

Long-term perfusion of liver grafts outside of the body may enable repair of poor-quality livers that are currently declined for transplantation, mitigating the global shortage of donor livers. In current ex vivo liver perfusion protocols, hyperoxic blood (arterial blood) is commonly delivered in the portal vein (PV). We perfused porcine livers for one week and investigated the effect of and mechanisms behind hyperoxia in the PV on hepatic arterial resistance. Applying PV hyperoxia in porcine livers (n = 5, arterial PV group), we observed an increased need for vasodilator Nitroprussiat (285 ± 162 ml/week) to maintain the reference hepatic artery flow of 0.25 l/min during ex vivo perfusion. With physiologic oxygenation (venous blood) in the PV the need for vasodilator could be reduced to 41 ± 34 ml/week (p = 0.011; n = 5, venous PV group). This phenomenon has not been reported previously, owing to the fact that such experiments are not feasible practically in vivo. We investigated the mechanism of the variation in HA resistance in response to blood oxygen saturation with a focus on the release of vasoactive substances, such as Endothelin 1 (ET-1) and nitric oxide (NO), at the protein and mRNA levels. However, no difference was found between groups for ET-1 and NO release. We propose direct oxygen sensing of endothelial cells and/or increased NO break down rate with hyperoxia as possible explanations for enhanced HA resistance.

Safety and efficacy of an integrated endovascular treatment strategy for early hepatic artery occlusion after liver transplantation.

BACKGROUND: Hepatic artery occlusion (HAO) after liver transplantation (LT) is typically comprised of hepatic artery thrombosis (HAT) and stenosis (HAS), both of which are severe complications that coexist and interdependent. This study aimed to evaluate an integrated endovascular treatment (EVT) strategy for the resolution of early HAO and identify the risk factors associated with early HAO as well as the procedural challenge encountered in the treatment strategy. METHODS: Consecutive orthotopic LT recipients (n = 366) who underwent transplantation between June 2017 and December 2018 were retrospectively investigated. EVT was performed using an integrated strategy that involved thrombolytic therapy, shunt artery embolization plus vasodilator therapy, percutaneous transluminal angioplasty, and/or stent placement. Simple EVT was defined as the clinical resolution of HAO by one round of EVT with thrombolytic therapy and/or shunt artery embolization plus vasodilator therapy. Otherwise, it was defined as complex EVT. RESULTS: Twenty-six patients (median age 52 years) underwent EVT for early HAO that occurred within 30 days post-LT. The median interval from LT to EVT was 7 (6-16) days. Revascularization time (OR = 1.027; 95% CI: 1.005-1.050; P = 0.018) and the need for conduit (OR = 3.558; 95% CI: 1.241-10.203, P = 0.018) were independent predictors for early HAO. HAT was diagnosed in eight patients, and four out of those presented with concomitant HAS. We achieved 100% technical success and recanalization by performing simple EVT in 19 patients (3 HAT+/HAS- and 16 HAT-/HAS+) and by performing complex EVT in seven patients (1 HAT+/HAS-, 4 HAT+/HAS+, and 2 HAT-/HAS+), without major complications. The primary assisted patency rates at 1, 6, and 12 months were all 100%. The cumulative overall survival rates at 1, 6, and 12 months were 88.5%, 88.5%, and 80.8%, respectively. Autologous transfusion < 600 mL (94.74% vs. 42.86%, P = 0.010) and interrupted suture for hepatic artery anastomosis (78.95% vs. 14.29%, P = 0.005) were more prevalent in simple EVT. CONCLUSIONS: The integrated EVT strategy was a feasible approach providing effective resolution with excellent safety for early HAO after LT. Appropriate autologous transfusion and interrupted suture technique helped simplify EVT.

Hyperspectral evaluation of hepatic oxygenation in a model of total vs. arterial liver ischaemia.

Liver ischaemia reperfusion injury (IRI) is a dreaded pathophysiological complication which may lead to an impaired liver function. The level of oxygen hypoperfusion affects the level of cellular damage during the reperfusion phase. Consequently, intraoperative localisation and quantification of oxygen impairment would help in the early detection of liver ischaemia. To date, there is no real-time, non-invasive, and intraoperative tool which can compute an organ oxygenation map, quantify and discriminate different types of vascular occlusions intraoperatively. Hyperspectral imaging (HSI) is a non-invasive optical methodology which can quantify tissue oxygenation and which has recently been applied to the medical field. A hyperspectral camera detects the relative reflectance of a tissue in the range of 500 to 1000 nm, allowing the quantification of organic compounds such as oxygenated and deoxygenated haemoglobin at different depths. Here, we show the first comparative study of liver oxygenation by means of HSI quantification in a model of total vascular inflow occlusion (VIO) vs. hepatic artery occlusion (HAO), correlating optical properties with capillary lactate and histopathological evaluation. We found that liver HSI could discriminate between VIO and HAO. These results were confirmed via cross-validation of HSI which detected and quantified intestinal congestion in VIO. A significant correlation between the near-infrared spectra and capillary lactate was found (r = - 0.8645, p = 0.0003 VIO, r = - 0.7113, p = 0.0120 HAO). Finally, a statistically significant negative correlation was found between the histology score and the near-infrared parameter index (NIR) (r = - 0.88, p = 0.004). We infer that HSI, by predicting capillary lactates and the histopathological score, would be a suitable non-invasive tool for intraoperative liver perfusion assessment.

Additional value of superb microvascular imaging for assessing hepatic arterial blood flow after pediatric liver transplantation.

BACKGROUND: The aim of this study was to explore the value of SMI compared with conventional ultrasonography for assessing hepatic arterial blood flow after pediatric liver transplantation. METHODS: From March 2018 to November 2018, a total of 105 pediatric recipients with biliary atresia underwent liver transplantation in our hospital. Ultrasound examinations were performed at the bedside in the intensive care unit to check the patency of the blood flow in the hepatic allograft. CDI, PDI, cSMI, and mSMI were performed to assess the display, orientation, and distribution of the graft hepatic artery. Ultrasound examinations were performed by one radiologist, and the images were judged by two observers. RESULTS: The median age, weight, and height of the recipients were 6.97 (5.92, 9.58) months, 6.50 (6.00, 7.80) kg, and 64.00 (62.00, 68.00) cm, respectively. The measure of kappa agreement was 0.902, 0.889, 0.882, and 0.882 for CDI, PDI, cSMI, and mSMI, respectively. HAT occurred in 7 pediatric recipients and was confirmed by CTA (computed tomography angiography) and surgery. The diagnostic performance of sensitivity, specificity, PPV (positive predictive value), NPV (negative predictive value), and accuracy were 100%, 92.86%, 50%, 100%, and 93.33% for CDI and 100%, 98.98%, 87.50%, 100%, and 99.05% for SMI. CONCLUSIONS: As an additional method to CDI, SMI can clearly show the distribution of hepatic arterial blood flow and provide more details, thereby markedly improving the diagnostic performance of postoperative HAT.

Intrahepatic Arterioportal Fistula: A Rare Cause of Portal Hypertension After Deceased Donor Liver Transplant.

A 43-year-old male patient, who received a deceased donor liver transplant for background ethanol-related decompensated cirrhosis, presented 7 months after transplant with mild abdominal distension and pain. On evaluation, the patient had thrombocytopenia, high serum-ascites albumin gradient ascites, and deranged liver functions. The Doppler study of the splenoportal axis showed hepatofugal flow in the recipient's portal vein, normal hepatic veins, a normal liver, splenomegaly, mild ascites, and multiple periportal collaterals. A transjugular liver biopsy and a hepatic venous pressure gradient measurement were done, which suggested mild portal tract inflammation with portal tract fibrosis with prominent portal venous thickening and normal hepatic venous pressure gradient (4 mm). However, the patient had a progressive increase in ascites and a dramatic increase in serum bilirubin level. A triple-phase computed tomography was done that showed rapid contrast flow in both the portal and hepatic arterial phase, suggesting arterialization of the portal flow with possible suspicion of a communicating arterioportal fistula. The patient underwent digital subtraction angiography, which was followed by an embolization of the arterioportal fistula. After embolization, serum bilirubin gradually decreased and ascites resolved. A repeat Doppler of the portal venous system showed established hepatopetal flow with progressively rising portal flow velocities.

Markedly elevated hepatic arterial velocity-HAV greater than 200 cm/s-is not specific to hepatobiliary disease.

OBJECTIVE: The aim of the study was to review the different etiologies and outcomes of patients with hepatic artery velocities greater than 200 cm/s. METHODS: This retrospective study included 88 hospitalized patients in whom angle-corrected proper hepatic artery flow velocities greater than 200 cm/s were obtained during an abdominal ultrasonographic examination. Peak systolic hepatic artery flow velocities, hepatic artery resistance index, and portal vein flow velocities were evaluated. The patients were then allocated to one of four groups based on their primary underlying diagnosis: structural liver disease, nonstructural liver disease, generalized infection, or miscellaneous. RESULTS: The median hepatic artery velocity was similar for all groups, ranging from 226 to 238 cm/s. The maximum portal venous velocities were not significantly different between groups. No lab values were statistically different between the groups, except total bilirubin that was greater in the nonstructural liver disease group (8 mg/dL). Overall, 9/88 (10.2%) of patients with elevated hepatic artery velocity died within 30 days of their ultrasonographic examination. CONCLUSION: Elevated hepatic artery velocity greater than 200 cm/s in hospitalized patients is not specific to primary hepatobiliary disease but may indicate acute hepatic dysfunction from other causes such as infection or sepsis.

A single-center clinical study of hepatic artery variations in laparoscopic pancreaticoduodenectomy: A retrospective analysis of data from 218 cases.

Hepatic artery variations increase the difficulty of laparoscopic pancreaticoduodenectomy (LPD). The safety and efficacy of LPD in the presence of aberrant hepatic arteries (AHA) must be further verified.Patients with normal and variant hepatic arteries who underwent LPD and preoperative arterial angiography were retrospectively analyzed. Variation type, intraoperative management, and clinical treatment outcomes were compared.There were 54 cases (24.8%) of AHA. The most common hepatic artery variation was accessory right hepatic artery (RHA) from the superior mesenteric artery (SMA, n = 12, 5.5%), followed by replaced RHA from the SMA (n = 10, 4.6%), accessory left hepatic artery from the SMA (n = 10, 4.6%), and replaced common hepatic artery from the SMA (n = 6, 2.8%). Each type of arterial variation was successfully preserved in all cases, and there were no significant effects on the evaluated surgical indices, conversion rate, incidence of postoperative complications, or follow-up results.Our findings indicated that preservation of AHAs during total LPD is feasible. There were no significant effects on surgical indices, incidence of postoperative complications, or follow-up outcomes.The influence of AHA on the safety and efficacy of LPD must be further verified. Patients with normal and variant hepatic arteries who underwent LPD and preoperative arterial angiography were retrospectively analyzed. There were 54 cases (24.8%) of AHA. There were no significant effects of AHAs on surgical indices, incidence of postoperative complications, or follow-up outcomes.

Management strategies for true and dissecting visceral artery aneurysms.

BACKGROUND: Visceral artery aneurysms (VAA) are rare and the literature regarding management strategies is limited. The study aim was to evaluate our 13-year experience with VAA treatment including conservative, open surgical and endovascular therapy. METHODS: This retrospective single-center study included 37 patients (31 male, median age 70 years [46-79 years]) with true and dissecting VAA treated between January 2006 and December 2018. Indications for invasive therapy were ruptured (N.=1) and symptomatic (N.=8) VAA or asymptomatic VAA>20 mm (N.=15). The decision on the treatment type was made after interdisciplinary (vascular surgeons/radiologists) discussion. RESULTS: The aneurysms affected the celiac trunk (N.=18, 49%), the splenic artery (N.=11, 30%), the superior mesenteric artery (SMA, N.=6, 16%), the hepatic artery (N.=5, 14%) and proximal SMA side branches (N.=2, 5%). Six patients had multiple VAA, one had an intrahepatic artery aneurysm and one had peripheral mesocolic artery aneurysms plus a VAA. 46% of the patients (N.=17) had coexisting aneurysms in other vascular territories. Thirteen patients were managed conservatively (median VAA diameter 15 [14-25] mm), 18 underwent open surgery with venous or prosthetic bypass or interposition graft implantation and 6 were treated by endovascular means (coiling [N.=3] or endograft [N.=3]). Median follow-up (FU) was 21 months (4-123 months). In-hospital mortality was 0%. Median length of hospital stay was 11 days (5-28 days) after surgical and 3 days (2-71 days) after endovascular treatment. Complications included an early type I endoleak, 3 secondary open abdominal surgeries for bleeding/peritonitis after endovascular treatment of a ruptured intrahepatic aneurysm, an asymptomatic aorto-truncal bypass occlusion and aneurysm recurrence after a venous SMA interposition graft. None of the conservatively treated VAA required invasive treatment during FU. CONCLUSIONS: Small (<20 mm) asymptomatic VAA can be managed conservatively. Whenever invasive treatment is indicated, both open and endovascular treatments can be performed with low complication rates. In order to choose the optimal therapeutic approach, anatomical features and patient comorbidities should be considered and, ideally, discussed interdisciplinarily.

Dissection of the Hepatic Artery: A Rare Cause of Late Ischemia After Liver Transplant.

Hepatic artery dissection is an infrequent vascular complication that can arise after orthotopic liver transplant. Most patients with this complication are diagnosed during the intraoperative period or the first days after liver transplant, with an association shown with living-donor liver transplant. In this study, we discuss a rare case of an extrahepatic artery dissection that was successfully managed through surgical excision and arterial revascularization that was diagnosed 4 years after orthotopic liver transplant. Furthermore, we hypothesize on the potential causes of its occurrence.