Liver Periphery Research Articles

Splenic Artery Syndrome After Orthotopic Liver Transplantation: Treatment With the Amplatzer Vascular Plug

To evaluate the safety and efficacy of the Amplatzer vascular plug (AVP) for embolization of the splenic artery in patients with hepatic hypoperfusion after orthotopic liver transplantation (OLT). Thirteen patients (9 men and 4 women) with a mean age of 56 years (range 22-70) who developed splenic artery syndrome after OLT with decreased liver perfusion and clinically relevant impairment of liver function (increased transaminase or serum bilirubin levels, thrombocytopenia, and/or therapy-refractory ascites) were treated by embolization of the proximal third of the splenic artery using the AVP. The plugs ranged in diameter from 6 to 16 mm, and they were introduced through femoral (n = 9), axillary (n = 3), or brachial (n = 1) access using a 5F or 8F guiding catheter. The plugs were successfully placed, and complete occlusion of the splenic artery was achieved in all patients. Placement of two plugs was necessary for complete occlusion in 3 of the 13 patients. Occlusion took on average 10 min (range 4-35). There was no nontarget embolization or plug migration into more distal segments of the splenic artery. All patients showed improved arterial perfusion, including the liver periphery, on postinterventional angiogram. After embolization, liver function parameters (transaminase and bilirubin levels) improved with normalization of concomitant thrombocytopenia and a decrease in ascites volume. Our initial experience in a small patient population with SAS suggests that the AVP enables precise embolization of the proximal splenic artery, thus providing safe and effective treatment for poor liver perfusion after OLT due to SAS.

Arterialised hepatic nodules in the Fontan circulation: Hepatico-cardiac interactions

Hypervascular nodules occur commonly when there is hepatic venous outlet obstruction. Their nature and determinants in the Fontan circulation is poorly understood. We reviewed the records of 27 consecutive Fontan patients who had computerized tomography scan (CT) over a 4year period for arterialised nodules and alterations in hepatic flow patterns during contrast enhanced CT scans and related these findings to cardiac characteristics. Mean patient age was 24±5.8years, (range 16.7–39.8) and mean Fontan duration was 16.8±4.8years (range 7.3–28.7). Twenty-two patients demonstrated a reticular pattern of enhancement, 4 a zonal pattern and only 1 demonstrated normal enhancement pattern. Seven (26%) patients had a median of 4 (range 1–22) arterialised nodules, mean size 1.8cm (range 0.5 to 3.2cm). All nodules were located in the liver periphery, their outer aspect lying within 2cm of the liver margin. Patients with nodules had higher mean RA pressures (18mmHg±5.6 vs. 13mmHg±4, p=0.025), whereas their mixed venous saturation and aortic saturation was not significantly different (70%±11 vs. 67%±9 and 92%±10 vs. 94%±4, p>0.05). Post-mortem histology suggests focal nodular hyperplasia is the underlying pathology. ConclusionsAbnormalities of hepatic blood flow and the presence of arterialised nodules are common in the failing Fontan circulation. They occur especially when central venous pressures are high, and very likely indicate arterialisation of hepatic blood flow and reciprocal portal venous deprivation. The underlying pathology is most likely focal nodular hyperplasia.

Fasciola-hepatica-Infektionen in der Schweiz – eine Fallserie

Described are the clinical and, especially, the contrast-enhanced ultrasonographic presentation and recovery of four cases of fascioliasis occurring between December 2008 and February 2009. A detailed history, clinical examination and laboratory investigation were followed by contrast-enhanced ultrasonography of the liver and serological evidence for the presence of antibodies. A final contrast-enhanced ultrasound was performed 6 weeks after treatment with triclabendazole. The patients displayed a variety of symptoms ranging from vasospastic myocardial infarction diagnosed via coronary angiography and a first-time occurrence of migraine as a result of hypereosinophilia to fever with weight loss and tumor-like liver lesions. The contrast-enhanced ultrasonographic hepatic changes in fascioliasis are characterized by segmental arterial hyperemia with emphasis on the liver periphery and subcapsular canalicular sparing corresponding to parenchymal necrosis and hemorrhage. In the later phases areas with inflammatory changes were unmasked due to phlebitis of the small portal vessels and granulomatous parenchymal changes. All four patients were successfully treated with triclabendazole without experiencing any serious side effects. Contrast-enhanced ultrasonography is well suited for the diagnosis and monitoring of hepatic fascioliasis.

Radiofrequency ablation of problematically located hepatocellular carcinoma: tailored approach

The challenge for radiofrequency ablation (RFA) of hepatocellular carcinomas (HCC) in problematic locations is that the outcome is limited due to insufficient ablation or injury of nearby structures. This study aimed to evaluate effective strategy and treatment results of RFA in these cases. Ultrasound guided percutaneous RFA was performed in 326 HCC patients. Among them, 249 tumors in 215 patients located at liver periphery, including 54 adjacent to GI tract, 110 close to the diaphragm, 49 close to the gallbladder, and 36 tumors close to liver surface. The sizes of the tumors ranged 1.2-7.0 cm (average 3.7 +/- 1.3 cm). Individualized treatment strategy was established for tumors in various locations, including "artificial ascites", "lift-expand" electrode placement, "draw-expand" electrode placement, "Supplementary ablation", and "accumulative multiple ablations" techniques. Treatment outcome was compared with another 64 central-located tumors (control group) in the same patients. One-month post-RFA contrast CT was used to evaluate early necrosis rate of the treated tumors. Early tumor necrosis were obtained in 91.6% (228/249) of the problematically located HCC, including 90.7% (49/54) of the tumors adjacent to GI tract, 90.9% (100/110) near the diaphragm, 91.8% (45/49) by the gallbladder, and 94.4% (34/36) close to liver surface. The necrosis rate of control group was 98.4% (63/64), which was higher than the tumors close to diaphragm (P = 0.049). Local tumor recurrence was 8.4% (21/249), comparing with 3.1% (2/64) of the control group (P > 0.05). The 1-, 2- and 3-year survival rate of this group were 81.6%, 63.8%, and 53.6%, respectively. Major complications occurred in 3.2% (11/343) of the treatment sessions, including hemorrhage in two, nearby structure injury in five, and needle tract seeding in four patients. Individualized treatment strategy for problematically located HCC is helpful in improving RFA outcome and expanding the application range of the therapy.

Peripheral Bile Duct Paucity and Cholestasis in the Liver of a Patient With Alagille Syndrome

Alagille syndrome (AGS) is a developmental, multiorgan disease caused by mutations of the Jagged1 gene. The liver is one of the major organs affected in AGS, and the hallmark of liver pathology in AGS is an age-related increase in the proportion of portal tracts that have no bile duct, but without evidence of prominent bile duct damage. The pathogenesis of this bile duct paucity is currently not well understood. (Immuno)histochemical and molecular analyses were performed on several liver biopsies that were taken during macroscopic examination of the explant liver of a 17-year-old AGS patient. The liver periphery was macroscopically pale and was microscopically characterized by complete absence of bile ducts and presence of severe cholestasis, but there was no ductular reaction. Conversely, the central, hilar portion contained normally developed bile ducts showing no or minimal damage and cholestasis. A missense mutation in the Jagged1 gene was present in both parts of the liver, indicating that mosaicism did not cause this peculiar picture. There was also a hypertrophy of the hepatic arterial branches in the liver periphery. Together with previous indirect findings, the current study of the explant liver of an AGS patient strongly suggests that a lack of branching and elongation of bile ducts during postnatal liver growth is the mechanism by which peripheral bile duct paucity and cholestasis develops in AGS. Our findings also suggest that anomalies of the intrahepatic arterial branches may be part of AGS in some patients.

Extension of Radiofrequency Ablation of the Liver by Transcatheter Arterial Embolization with Iodized Oil and Gelatin Sponge: Results in a Pig Model

To determine whether transcatheter arterial embolization (TAE) with iodized oil and gelatin sponge particles can be used to expand radiofrequency (RF)-induced coagulation necrosis, the morphology and histologic characteristics of ablation lesions were evaluated in the normal pig liver after three different TAE procedures. Ten consecutive animals with 33 ablation lesions produced with an RF ablation system were randomly assigned to one of three treatment groups and a control group: a group treated with TAE with iodized oil, a group treated with TAE with gelatin sponge, a group treated with TAE with iodized oil and gelatin sponge, and a control group in which TAE was not performed. After the completion of ablation, the lesions were excised for gross and histologic examination. The longest and shortest diameters of ablation lesions were greatest in the group treated with TAE with iodized oil and gelatin sponge, followed by the groups treated with TAE with gelatin sponge and TAE with iodized oil (P < .05 vs controls, respectively). The hemorrhagic rim was also widest in the group treated with TAE with iodized oil and gelatin sponge (P < .05 vs controls), and it spread toward the liver periphery like a segmental hemorrhagic area adjacent to the ablation lesion. Histochemical staining for lactate dehydrogenase, maleate dehydrogenase, and nicotinamide adenine dinucleotide diaphorase showed what appeared to be 100% cellular destruction in all the ablation lesions and their hemorrhagic rims. RF ablation combined with TAE with iodized oil and gelatin sponge induces the greatest area of coagulation necrosis accompanied by peripherally spreading segmental necrosis in normal pig liver tissue.

Microvascular Origin of Laser-Doppler Flux Signal from the Surface of Normal and Injured Liver of the Rat

Although laser-Doppler flowmetry (LDF) is a widely used technique, little is known about its microvascular origin from the surface of the liver. In the present study, we attempted to identify the microvascular bed interrogated by the laser light, by correlating perfusion and red blood cell velocity data obtained using intravital fluorescence microscopy (IVFM) with the LDF signal recorded under normal conditions and following liver injury. Sprague–Dawley rats which underwent hepatic artery ligation (HAL) or nonarterialized liver transplantation (NOLT) served as in vivo models of reduced sinusoidal red blood cell velocity (RBCvel) and altered homogeneity of perfusion, respectively. Three groups of animals were studied: HAL (n = 8), NOLT (n = 8), and sham-operated control (n = 8). Homogeneous perfusion of the sinusoids and liver lobules and reduced sinusoidal RBCvel were initially confirmed in the HAL group. In addition, significantly reduced sinusoidal and lobular perfusion was observed in the NOLT liver. HAL caused a 28% reduction in the LDF signal (P < 0.05 vs sham), whereas the LDF signal from the NOLT liver (101 ± 11 PU) was lower than that from the native recipient liver with HAL (128 ± 11 PU). Under control conditions, and following HAL and NOLT, a linear correlation could be established only between sinusoidal RBCvel and LDF signal (y = 0.78x + 50.98, r2 = 0.71, P < 0.001). Furthermore, using IVFM images and NIH Image analysis, we estimated a high contribution of the sinusoids to the total vascular space at the liver periphery. Our data indicate that under normal conditions and those of altered microcirculation, blood flow in the sinusoids, compared to other microvessels, has a significant influence on the LDF signal from the surface of the liver.

Extracranial radiosurgery: Immobilizing liver motion in dogs using high-frequency jet ventilation and total intravenous anesthesia

Purpose: Extracranial radiosurgery requires control of organ motion. The purpose of this study is to quantitatively determine the extent of liver motion in anesthetized dogs with continuous i.v. propofol infusion with or without muscle relaxants and high-frequency jet ventilation. Methods and Materials: Five dogs were used in the experiment. Each dog was restrained while anesthetized in the supine position using an alpha cradle. Surgical metal clips were implanted around the liver periphery so that its motion could be visualized using a fluoroscopic imaging device in a conventional simulator. Initially, two orthogonal simulation films were taken to correlate locations of implanted clips. Two orthogonal views of fluoroscopic images for each anesthetized dog were recorded on a magnetic tape and analyzed from the post-imaging data. Liver motion was documented under the following three conditions: 1) ventilated with a conventional mechanical ventilator, 2) ventilated with a high-frequency jet ventilator, and 3) ventilated with a high-frequency jet ventilator and total muscle paralysis (with vecuronium injection). The maximum liver motion for each dog was analyzed in three orthogonal directions: the inferior-to-superior direction, the anterior-to-posterior direction, and the right-to-left direction. Results: When the anesthetized dogs were ventilated with a conventional mechanical ventilator, the average liver motions were 1.2 cm in the inferior-to-superior direction, 0.4 cm in the anterior-to-posterior direction, and 0.2 cm in the right-to-left direction, respectively. After the introduction of high-frequency jet ventilation, the average liver motions were reduced to 0.2 cm in the inferior-to-superior direction, 0.2 cm in the anterior-to-posterior direction, and 0.1 cm in the right-to-left direction. The maximum liver motion was dependent on ventilator settings. There was no additional measurable motion reduction with the addition of the muscle relaxant. Conclusion: The liver motion in each anesthetized dog was controlled under 3.0 mm in all directions with the use of high-frequency jet ventilation. No detectable advantage was identified by the injection of muscle relaxant in terms of further reducing the liver motion. The preclinical animal study indicated that the use of high-frequency jet ventilation (HFJV) would be able to limit the liver motion to an extent acceptable for the application of extracranial radiosurgery in humans. Radiosurgery for localized liver tumors warrants further investigation.

Budd-Chiari syndrome: spectrum of appearances of acute, subacute, and chronic disease with magnetic resonance imaging.

The purpose of this study was to describe our collective experience in the magnetic resonance (MR) investigation of patients with proven acute, subacute, and chronic Budd-Chiari syndrome and to demonstrate the spectrum of appearances on T1- and T2-weighted as well as dynamic post-gadolinium spoiled gradient-echo imaging. All patients with proven Budd-Chiari syndrome who underwent MR examinations between June, 1992 and October, 1998 were included in the study. Fourteen patients were included in the study: four with acute, three with subacute, three with chronic, and four with acute superimposed on either subacute (two) or chronic (two) Budd-Chiari syndrome. MR imaging features were retrospectively evaluated to determine: a) liver morphology, b) pattern of signal intensity (SI) on T1-weighted images, c) pattern of SI on T2 weighted images, d) dynamic enhancement characteristics, e) presence or absence of visible venous thrombosis, and f) presence or absence of venous macroscopic collaterals. The MR findings were correlated with surgical, histopathological, and laboratory data to determine imaging characteristics related to the chronicity of the disease process. Hepatic venous thrombosis or absence of hepatic venous flow was demonstrated in all patients in the study. In the four patients with acute Budd-Chiari syndrome, the liver periphery was moderately low signal on T1 and moderately high signal on T2-weighted images relative to the central liver; both early and late gadolinium-enhanced images revealed diminished peripheral enhancement. In the three patients with subacute Budd-Chiari syndrome, the liver periphery was moderately low signal on T1, and moderately high signal on T2-weighted images, while early and late gadolinium-enhanced images revealed heterogenously increased enhancement within the liver periphery. In the three patients with chronic Budd-Chiari syndrome, the SI differences between peripheral and central liver were minimal on T1- and T2-weighted images, and enhancement differences were also minimal. Extensive bridging intrahepatic and capsular venous collaterals were visualized in chronic cases. In the four patients with acute Budd-Chiari syndrome superimposed on more chronic disease, a combination of gadolinium enhancement patterns was observed on MR images. Enhancement patterns between central and peripheral liver were different for acute, subacute, and chronic Budd-Chiari syndromes, suggesting differentiation between these phases of the disease process. Application of this pattern approach permitted recognition of acute changes superimposed on more chronic disease.

Budd-chiari syndrome: Spectrum of appearances of acute, subacute, and chronic disease with magnetic resonance imaging

The purpose of this study was to describe our collective experience in the magnetic resonance (MR) investigation of patients with proven acute, subacute, and chronic Budd-Chiari syndrome and to demonstrate the spectrum of appearances on T1- and T2-weighted as well as dynamic post-gadolinium spoiled gradient-echo imaging. All patients with proven Budd-Chiari syndrome who underwent MR examinations between June, 1992 and October, 1998 were included in the study. Fourteen patients were included in the study: four with acute, three with subacute, three with chronic, and four with acute superimposed on either subacute (two) or chronic (two) Budd-Chiari syndrome. MR imaging features were retrospectively evaluated to determine: a) liver morphology, b) pattern of signal intensity (SI) on T1-weighted images, c) pattern of SI on T2 weighted images, d) dynamic enhancement characteristics, e) presence or absence of visible venous thrombosis, and f) presence or absence of venous macroscopic collaterals. The MR findings were correlated with surgical, histopathological, and laboratory data to determine imaging characteristics related to the chronicity of the disease process. Hepatic venous thrombosis or absence of hepatic venous flow was demonstrated in all patients in the study. In the four patients with acute Budd-Chiari syndrome, the liver periphery was moderately low signal on T1 and moderately high signal on T2-weighted images relative to the central liver; both early and late gadolinium—enhanced images revealed diminished peripheral enhancement. In the three patients with subacute Budd-Chiari syndrome, the liver periphery was moderately low signal on T1, and moderately high signal on T2-weighted images, while early and late gadolinium-enhanced images revealed heterogenously increased enhancement within the liver periphery. In the three patients with chronic Budd-Chiari syndrome, the SI differences between peripheral and central liver were minimal on T1- and T2-weighted images, and enhancement differences were also minimal. Extensive bridging intrahepatic and capsular venous collaterals were visualized in chronic cases. In the four patients with acute Budd-Chiari syndrome superimposed on more chronic disease, a combination of gadolinium enhancement patterns was observed on MR images. Enhancement patterns between central and peripheral liver were different for acute, subacute, and chronic Budd-Chiari syndromes, suggesting differentiation between these phases of the disease process. Application of this pattern approach permitted recognition of acute changes superimposed on more chronic disease. J. Magn. Reson. Imaging 2000;11:44–50. © 2000 Wiley-Liss, Inc.

Liver regeneration after partial hepatectomy is non-uniform: flow cytometric bromodeoxyuridine incorporation and cell cycle studies in a porcine model.

The rate of hepatocyte regeneration at different anatomical locations of the remnant liver after partial hepatectomy was assessed in porcine hepatocytes by bromodeoxyuridine (BrdUr) incorporation and cell cycle kinetics using flow cytometric analysis. Partial hepatectomy was performed in five Yorkshire pigs. A single intravenous injection of BrdUr at 50 mg/kg was administered on the 2nd post-operative day and the animals were sacrificed 1 h later. The remnant liver tissue was harvested and divided into four equal zones, from the liver periphery towards the surgical cut-edge. Biopsy samples were obtained from the centre of each of these zones and similarly from identical anatomical locations in two control pigs that had undergone sham surgery. Hepatocyte nucleus suspension was prepared, double labelled with anti-BrdUr and propidium iodide and analysed by a flow cytometer. The cells in S-phase was used as the parameter to measure the regeneration status. A gradient increase in S-phase from the periphery to the cut edge was observed in all five pigs that had undergone partial hepatectomy. The percentage of S-phase cells in all four zones from the hepatectomy group was significantly higher when compared with that in the controls. Liver regeneration after partial hepatectomy was not uniform but was greatest adjacent to the surgical cut edge and decreased towards the periphery of the liver.

A method to perfuse liver metastases with heated blood (45 �C, 45 min)

To heat the livers in ten pigs (20-30 kg) a system of two pumps, both connected to the cannulated A.femoralis and to two radio-wave heating devices, was used. With pump I the arterial vascular system of the liver was perfused for 45 min via the A.gastroduodenalis with a constant volume of 150-200 ml blood/min, heated to 44-45 degrees C. With pump II 50-700 ml/min heated blood was pumped into the portal vein to raise the temperature and oxygen content of the portal flow. During the heating period the A.hepatica was clamped. A temperature of 45 degrees C is a highly toxic for the differentiated liver tissue, but the more simply structured wall of the arteries tolerates this temperature. This difference in heat resistance allows the perfusion of the arterial vascular system of the liver with blood heated to a temperature that is fatal to liver tissues. On the way from the A.gastroduodenalis to the liver periphery the heated blood becomes cooled by the surrounding cooler liver tissues. Finally the supply to the lobules is a mixture of arterial and venous blood, i.e. the highly toxic agent, heat, becomes "detoxified" by cooling before reaching the heat-sensitive liver lobules. Changing flow and temperature in the portal vein allows the temperature of the liver lobules to be kept within a safe range, i.e. below 43 degrees C. The raised oxygen content in the portal flow allows the arterial perfusion to be stopped for 10 min (to subject a heated metastasis to a period of hypoxia). Liver enzymes reached their maximal level 2 days after heating and returned to normal within 1 week. It is supposed that this method allows the temperature in a liver metastasis to be raised to a tumoricidal level.

Peribiliary plexa--important pathways for shunting of iodized oil and silicon rubber solution from the hepatic artery to the portal vein. An experimental study in rats.

Iodized oil is commonly used in chemoembolization of hepatic tumors, and silicon rubber solution is used for casting studies of hepatic tumor vasculature. Understanding the distribution patterns of iodized oil and silicon rubber solution is of significance in the refinement of iodized oil techniques and proper interpretation of hepatic tumor vascular studies. In this study, the location for iodized oil and silicon rubber solution shunting from the hepatic artery to the portal vein was identified. Iodized oil and silicone rubber solution were injected into the hepatic artery in rats. The porta hepatis and the liver periphery were examined using in vivo microscopy. Iodized oil and silicone rubber solution had identical distribution patterns in the hepatic circulation. Both were shunted in large quantities from the hepatic artery into the portal vein through the peribiliary plexa. Other potential shunting sites did not contribute to the shunting. Though of different chemical natures, iodized oil and silicon rubber solution share similar distribution patterns in the liver. Hepatic arterioportal shunting of these substances occurs via the peribiliary plexa.