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Author: Grafiati

Published: 11 March 2023

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1

Bridwell, Rachel E., Sean Clerkin, Nathaniel R. Walker, Brit Long, and Sarah Goss. "Portal Venous Thrombosis in a Special Operations Paratrooper: A Case Report." Military Medicine 187, no. 1-2 (September 30, 2021): 256–58. http://dx.doi.org/10.1093/milmed/usab387.

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ABSTRACT Portal vein thrombosis is the thrombotic occlusion of the extrahepatic portal system, which can propagate towards the vena caval system. Although rare, it occurs primarily in those with cirrhosis, intra-abdominal infections, malignancy, or hypercoagulable disorders. This report describes the first reported case of a soldier within special operations without identifiable risk factors who was found to have a completely occlusive portal vein thrombosis after approximately 10 days of insidious abdominal pain. This case emphasizes the importance of considering this rare but dangerous pathology among this highly screened and capable special operations population.

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2

Iqbal, Nabeela, Syed Khalid Shah, and Shamima Haneef. "Polycythemia Vera Complicated by Portal Vein Thrombosis and Budd-Chiari Syndrome:." Journal of Bahria University Medical and Dental College 10, no. 02 (March 18, 2021): 163–65. http://dx.doi.org/10.51985/jbumdc2020019.

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Polycythemia vera is a medical condition characterized by raised hematocrit. Owing to increased viscosity, the blood flow in the vessels become sluggish leading to the clinical features of polycythemia such as headache, blurring of vision, red skin, dizziness, raised blood pressure, itching and more serious medical events like vaso occlusion, thrombosis and strokes. In this case report, polycythemia vera presenting unusually with heamatemesis, melena and abdominal distension. Physical examination of this case revealed massive ascites with dilated veins around the umbilicus. The diagnosis of polycythemia vera complicated by Budd Chiari Syndrome and Portal Vein Thrombosis was made. Patients with polycythemia vera are at risk of vaso occlusive sequelea like portal vein thrombosis and Budd chiari syndrome

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3

Strbe, Sanja, Slaven Gojkovic, Ivan Krezic, Helena Zizek, Hrvoje Vranes, Ivan Barisic, Dean Strinic, et al. "Over-Dose Lithium Toxicity as an Occlusive-like Syndrome in Rats and Gastric Pentadecapeptide BPC 157." Biomedicines 9, no. 11 (October 20, 2021): 1506. http://dx.doi.org/10.3390/biomedicines9111506.

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Due to endothelial impairment, high-dose lithium may produce an occlusive-like syndrome, comparable to permanent occlusion of major vessel-induced syndromes in rats; intracranial, portal, and caval hypertension, and aortal hypotension; multi-organ dysfunction syndrome; brain, heart, lung, liver, kidney, and gastrointestinal lesions; arterial and venous thrombosis; and tissue oxidative stress. Stable gastric pentadecapeptide BPC 157 may be a means of therapy via activating loops (bypassing vessel occlusion) and counteracting major occlusion syndromes. Recently, BPC 157 counteracted the lithium sulfate regimen in rats (500 mg/kg/day, ip, for 3 days, with assessment at 210 min after each administration of lithium) and its severe syndrome (muscular weakness and prostration, reduced muscle fibers, myocardial infarction, and edema of various brain areas). Subsequently, BPC 157 also counteracted the lithium-induced occlusive-like syndrome; rapidly counteracted brain swelling and intracranial (superior sagittal sinus) hypertension, portal hypertension, and aortal hypotension, which otherwise would persist; counteracted vessel failure; abrogated congestion of the inferior caval and superior mesenteric veins; reversed azygos vein failure; and mitigated thrombosis (superior mesenteric vein and artery), congestion of the stomach, and major hemorrhagic lesions. Both regimens of BPC 157 administration also counteracted the previously described muscular weakness and prostration (as shown in microscopic and ECG recordings), myocardial congestion and infarction, in addition to edema and lesions in various brain areas; marked dilatation and central venous congestion in the liver; large areas of congestion and hemorrhage in the lung; and degeneration of proximal and distal tubules with cytoplasmic vacuolization in the kidney, attenuating oxidative stress. Thus, BPC 157 therapy overwhelmed high-dose lithium intoxication in rats.

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4

Wang, L. Q., B. G. Persson, and S. Bengmark. "The Influence of Portal Deviation on the Effect of Repeat Dearterializations of a Transplantable Adenocarcinoma to the Rat Liver." HPB Surgery 8, no. 1 (January 1, 1994): 37–41. http://dx.doi.org/10.1155/1994/68212.

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As liver tumours receive some of their blood supply from the portal vein, we wanted to illustrate the influence of portal blood flow in combination with dearterialization in the treatment of liver tumours. Forty male, inbred Wistar/Furth rats with an adenocarcinoma transplanted to the liver were treated with various inflow occlusions repeated daily for 5 days. Deviation of the portal blood flow alone with an end-side porto-caval shunt did not alter the tumour growth (p = 0.089). Thirty min of repeat dearterializations was potentiated by portal deviation so that tumour growth was delayed (p = 0.004). However, repeat dearterializations for 60 min in portal deviated rats induced irreversible liver damage and all rats died in a few days. Repeated dearterializations for 60 minutes alone retarded the tumour growth as efficiently (p = 0.007). Simultaneous occlusion of the hepatic artery and the portal vein for 30 minutes with a side-side porto-caval shunted (total devascularization) did not affect tumour growth (p = 0.154). Liver aminotransferases (ASAT and ALAT) were substantially increased following dearterialization for 30 min in rats with either an end-side or a side-side porto-caval shunt. Dearterialization for 60 min in rats with end-side porto-caval shunts gave a further release of ASAT and ALAT.In conclusion, portal deviation did not augment the therapeutic benefit of repeat dearterializations for the treatment of this experimental liver tumour. Repeat dearterializations alone seemed to be a feasible and efficient therapy for liver tumours.

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5

Marn, C. S., and I. R. Francis. "CT of portal venous occlusion." American Journal of Roentgenology 159, no. 4 (October 1992): 717–26. http://dx.doi.org/10.2214/ajr.159.4.1326882.

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6

Shibamoto, Toshishige, Sen Cui, Zonghai Ruan, Wei Liu, Hiromichi Takano, and Yasutaka Kurata. "Hepatic venoconstriction is involved in anaphylactic hypotension in rats." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 4 (October 2005): H1436—H1441. http://dx.doi.org/10.1152/ajpheart.00368.2005.

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We determined the roles of liver and splanchnic vascular bed in anaphylactic hypotension in anesthetized rats and the effects of anaphylaxis on hepatic vascular resistances and liver weight in isolated perfused rat livers. In anesthetized rats sensitized with ovalbumin (1 mg), an intravenous injection of 0.6 mg ovalbumin caused not only a decrease in systemic arterial pressure from 120 ± 9 to 43 ± 10 mmHg but also an increase in portal venous pressure that persisted for 20 min after the antigen injection (the portal hypertension phase). The elimination of the splanchnic vascular beds, by the occlusions of the celiac and mesenteric arteries, combined with total hepatectomy attenuated anaphylactic hypotension during the portal hypertension phase. For the isolated perfused rat liver experiment, the livers derived from sensitized rats were hemoperfused via the portal vein at a constant flow. Using the double-occlusion technique to estimate the hepatic sinusoidal pressure, presinusoidal ( Rpre) and postsinusoidal ( Rpost) resistances were calculated. An injection of antigen (0.015 mg) caused venoconstriction characterized by an almost selective increase in Rpre rather than Rpost and liver weight loss. Taken together, these results suggest that liver and splanchnic vascular beds are involved in anaphylactic hypotension presumably because of anaphylactic presinusoidal contraction-induced portal hypertension, which induced splanchnic congestion resulting in a decrease in circulating blood volume and thus systemic arterial hypotension.

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7

Terada, N., S. Koyama, J. Horiuchi, and T. Takeuchi. "Participation of adrenoceptors in liver blood flow regulation in anesthetized dogs." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 5 (November 1, 1987): H1053—H1058. http://dx.doi.org/10.1152/ajpheart.1987.253.5.h1053.

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We evaluated involvement of adrenergic receptors in the responses of the hepatic vasculature to reduction either of portal venous flow or hepatic arterial inflow. Portal vein occlusion caused an increase in hepatic arterial blood flow (HAF) and decreases in hepatic arterial pressure (HAP) and hepatic arterial vascular resistance (HAR) in the intact group. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the portal vein produced a greater decrease in HAP as compared with that in the intact group. No significant changes in HAF, HAR, or hepatic tissue blood flow (HTF) occurred after the treatment. These results indicate that the compensatory response of the hepatic arterial vasculature to altered portal blood flow (PVF) is regulated independently of the intrahepatic adrenergic receptors. Hepatic arterial occlusion caused a significant decrease in portal venous pressure, PVF, and HTF. Portal venous vascular resistance (PVR) was reduced slightly, but not significantly. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the hepatic artery produced an opposite effect: to increase PVF and significantly decrease PVR. These results indicate that intrahepatic alpha-adrenoceptors participate in the regulation of portal vascular tone to maintain portal vein pressure at a steady level, when inflow from the hepatic artery is reduced.

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8

Kamikado, Chiaki, Toshishige Shibamoto, Minoru Hongo, and Shozo Koyama. "Effects of Hct and norepinephrine on segmental vascular resistance distribution in isolated perfused rat livers." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 1 (January 2004): H121—H130. http://dx.doi.org/10.1152/ajpheart.01136.2002.

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We studied the effects of blood hematocrit (Hct), blood flow, or norepinephrine on segmental vascular resistances in isolated portally perfused rat livers. Total portal hepatic venous resistance ( Rt) was assigned to the portal ( Rpv), sinusoidal ( Rsinus), and hepatic venous ( Rhv) resistances using the portal occlusion (Ppo) and the hepatic venous occlusion (Phvo) pressures that were obtained during occlusion of the respective line. Four levels of Hct (30%, 20%, 10%, and 0%) were studied. Rpv comprises 44% of Rt, 37% of Rsinus, and 19% of Rhv in livers perfused at 30% Hct and portal venous pressure of 9.1 cmH2O. As Hct increased at a given blood flow, all three segmental vascular resistances of Rpv, Rsinus, and Rhv increased at flow >15 ml/min. As blood flow increased at a given Hct, only Rsinus increased without changes in Rpv or Rhv. Norepinephrine increased predominantly Rpv, and, to a smaller extent, Rsinus, but it did not affect Rhv. Finally, we estimated Ppo and Phvo from the double occlusion maneuver, which occluded simultaneously both the portal and hepatic venous lines. The regression line analysis revealed that Ppo and Phvo were identical with those measured by double occlusion. In conclusion, changes in blood Hct affect all three segmental vascular resistances, whereas changes in blood flow affect Rsinus, but not Rpv or Rhv. Norepinephrine increases mainly presinusoidal resistance. Ppo and Phvo can be obtained by the double occlusion method in isolated perfused rat livers.

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9

Bayraktar, Yusuf, Abdurrahman Kadayifci, Ferhun Balkanci, Burhan Kayhan, David H. Van Thiel, and Sevket Ruacan. "Splenic Artery Occlusion Masking Portal Hypertension." Journal of Clinical Gastroenterology 22, no. 4 (June 1996): 326–28. http://dx.doi.org/10.1097/00004836-199606000-00021.

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10

Cheng, Yu Fan, Chien Fu Hung, Yang Han Liu, Koon Kwan Ng, and Chung Chueng Tsai. "Hepatic actinomycosis with portal vein occlusion." Gastrointestinal Radiology 14, no. 1 (December 1989): 268–70. http://dx.doi.org/10.1007/bf01889213.

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11

Sauerbuch (Discussion Leader), Tilman, Ulrich T. Hopt, Hannes Neeff, Bernd Pötzsch, Martin Rössle, and Dominique Valla. "Management of Portal/Mesenteric Vein Occlusion." Viszeralmedizin 30, no. 6 (2014): 2. http://dx.doi.org/10.1159/000369153.

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12

Unno, Naoki, Takashi Uchiyama, Naoto Yamamoto, Kazunori Inuzuka, Daisuke Sagara, and Hiroyuki Konno. "Portal Triad Occlusion Induces Endotoxin Tolerance: Role of Portal Congestion." Journal of Surgical Research 135, no. 2 (October 2006): 213–17. http://dx.doi.org/10.1016/j.jss.2006.03.042.

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13

Park, D. J., and J. S. Heo. "Portal vein stenting for symptomatic portal vein occlusion after pancreaticoduodenectomy." HPB 20 (September 2018): S631. http://dx.doi.org/10.1016/j.hpb.2018.06.2215.

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14

Alfidja, A., A. Abergel, P. Chabrot, D. Pezet, C. Bony, A. Ravel, J. M. Garcier, A. Roche, and L. Boyer. "Portal vein stenosis and occlusion stenting after liver transplantation in two adults." Acta Radiologica 47, no. 2 (March 2006): 130–34. http://dx.doi.org/10.1080/02841850500444705.

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We report two cases of percutaneous transhepatic stenting of the portal vein to treat stenosis and occlusion disclosed 5 and 18 months, respectively, after orthotopic liver transplantation in two adult patients. If long-term patency is satisfactory, this technique should allow long-term management of portal vein stenosis and occlusion without the use of thrombolysis.

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15

Jeppsson, Bengt. "Liver Resection: Prolonged Inflow Occlusion in Human Cirrhotic Livers." HPB Surgery 10, no. 2 (January 1, 1996): 123–25. http://dx.doi.org/10.1155/1996/45405.

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To evaluate the tolerance of the cirrhotic liver to extended warm ischaemia, 47 patients with cirrhosis who underwent liver,resection over a 4-year period were studied retrospectively. Three groups of patients were identified. In group 1 (14 patients) liver resection was performed under conditions of portal triad occlusion ranging from 50 to 75 (mean 57.1) min. Group 2 (12 patients) was treated with portal occlusion for a period ranging from 30 to 42 (mean 33.1) min. Group 3 comprised 21 patients who underwent hepatectomy using conventional techniques. Mean blood loss was significantly reduced by portal triad occlusion (819 ml in group 1,523 ml in group 2) compared with the conventional techniques (1652 ml in group 3) (P<0.05, group 1 versus group 3; P<0.01, group 2 versus group 3). Hospital death occurred in three of the 21 patients in group 3 but in no patient who underwent portal triad occlusion. The morbidity rate was lower in the two occlusion groups (four of 26 patients) than in group 3 (six of 21). Bilirubin metabolism was substantially better after surgery in the occlusion groups (P<0.05, groups 1 and 2 versus group 3 at day 14). Although the serum levels of transaminases were significantly raised until day 3 in patients undergoing long term occlusion, the cirrhotic liver withstood the ischaemia-reperfusion insult, as assessed by changes in hepatic microcirculation, lipid peroxidation and the morphology of hepatic sinusoids. It is concluded that prolonged ischaemia during liver resection can be sustained in patients with cirrhosis and without high-risk factors.

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16

Jakab, F., Z. Ráth, F. Schmal, P. Nagy, and J. Faller. "A New Method to Measure Portal Venous and Hepatic Arterial Blood Flow Patients Intraoperatively." HPB Surgery 9, no. 4 (January 1, 1996): 239–43. http://dx.doi.org/10.1155/1996/15760.

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The intraoperative measurement of the afferent circulation of the liver, namely the hepatic artery flow and portal venous flow was carried out upon 14 anesthetized patients having carcinoma in the splanchnic area, mainly in the head of the pancreas by means of transit time ultrasonic volume flowmeter. The hepatic artery flow, portal venous flow and total hepatic flow were 0.377±0.10; 0.614±0.21; 0.992±0.276 l/min respectively.The ratio of hepatic arterical flow to portal venous flow was 0.66±0.259 There was a sharp, significant increase in hepatic arterial flow (29.8±6.1%, p<0,01) after the temporary occlusion of the portal vein, while the temporary occlusion of hepatic artery did not have any significant effect on portal venous circulation. The interaction between hepatic arterial flow and portal venous flow is a much disputed question, but according to the presented data here, it is unquestionable, that the decrease of portal venous flow immediately results a significant increase in hepatic artery circulation.

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17

Hauenstein, Karlheinz, and Yan Li. "Radiological Diagnosis of Portal/Mesenteric Vein Occlusion." Viszeralmedizin 30, no. 6 (2014): 382–87. http://dx.doi.org/10.1159/000370055.

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18

Duminuco, Andrea, Alessandra Cupri, Rosario Massimino, Salvatore Leotta, Giulio Antonio Milone, Bruno Garibaldi, Giulia Giuffrida, Orazio Garretto, and Giuseppe Milone. "Handheld Ultrasound or Conventional Ultrasound Devices in Patients Undergoing HCT: A Validation Study." Journal of Clinical Medicine 12, no. 2 (January 8, 2023): 520. http://dx.doi.org/10.3390/jcm12020520.

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Abdominal ultrasound exams play a major role in the diagnosis of sinusoidal obstruction syndrome/veno-occlusive disease (SOS/VOD). The development of portable hand-held ultrasound devices (HHUS) has been shown to facilitate the diagnosis of many diseases, but little data on the value of HHUS in the diagnosis of SOS/VOD are available. We performed a study aimed at validating portable ultrasound (US) devices in the setting of hematopoietic stem cell transplant (HCT). Sixteen evaluable patients undergoing allogeneic HCT were studied using conventional US and HHUS during the first 3 weeks after transplant. The results obtained demonstrate that there is a close correlation between conventional and handheld ultrasound examination in the measurement of the right hepatic lobe (r = 0.912, p < 0.0001), the left hepatic lobe (r = 0.843, p < 0.0001), the portal vein (PV) (r = 0.724, p < 0.0001), and the spleen (r = 0.983, p < 0.0001) based on Pearson’s correlation. The same data, analyzed through Lin’s concordance correlation coefficient, evidenced a substantial level of agreement in the comparison of the spleen and right hepatic lobe, while a lower grade of agreement in the measurement of the portal vein and left hepatic lobe. Moreover, there was good agreement between results obtained by the two types of ultrasound devices in assessing ascites (p < 0.0001), gallbladder thickening (p < 0.0001), and the direction of PV flow (p < 0.0001). HHUS device allows the study of HokUs-10 parameters with an excellent agreement with conventional US, and may contribute to SOS/VOD diagnosis.

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19

Ausania, F., R. Jackson, T. Tsirlis, and RM Charnley. "Portal vein occlusion following pancreaticoduodenectomy and portal vein resection: treatment by percutaneous portal vein stent." Annals of The Royal College of Surgeons of England 95, no. 4 (May 2013): 299. http://dx.doi.org/10.1308/rcsann.2013.95.4.299.

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20

Youssef, E., M. Ghosn, M. El Hawari, G. Fine, M. Maybody, H. Yarmohammadi, K. Brown, and F. Boas. "Abstract No. 214 Portal vein stent placement for malignant portal vein occlusion." Journal of Vascular and Interventional Radiology 33, no. 6 (June 2022): S98—S99. http://dx.doi.org/10.1016/j.jvir.2022.03.295.

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21

Yada, Shinichiro, Kazuoki Hizawa, Kunihiko Aoyagi, Makoto Hashizume, Takayuki Matsumoto, Hideki Koga, and Masatoshi Fujishima. "PORTAL HYPERTENSIVE GASTROPATHY DUE TO CHRONIC PORTAL VEIN OCCLUSION IN CROHN'S DISEASE." American Journal of Gastroenterology 93, no. 8 (August 1998): 1376–77. http://dx.doi.org/10.1111/j.1572-0241.1998.424_e.x.

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22

Liu, Lexin, B. Jeppsson, and S. Bengmark. "Bacterial Translocation into Portal Blood from the Gut during Portal Triad Occlusion." Digestive Surgery 9, no. 2 (1992): 95–101. http://dx.doi.org/10.1159/000172068.

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23

Koós, Olivér, Tibor Kovács, András Fülöp, Damján Pekli, Péter Ónody, Péter Lukovich, László Harsányi, Péter Kupcsulik, Oszkár Hahn, and Attila Szijártó. "A posztoperatív keringésváltozások jelentősége a májsebészetben." Orvosi Hetilap 156, no. 48 (November 2015): 1938–48. http://dx.doi.org/10.1556/650.2015.30289.

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There are two afferent (hepatic artery, portal vein) and one efferent (hepatic veins) systems responsible for the unique circulation of the liver. Given this special form of vasculature, acute, isolated (i.e. involving selectively one particular vessel) vascular occlusions may lead to different, however still life threatening conditions. Hence, it is essential to recognize these anomalies in order to preserve the healthy state of both the liver and the patient’s lives. Acute circulatory failures are dominantly associated with liver surgery. Adequate therapy can only be provided promptly, if the clinician is well aware of the peculiarities of these conditions. The aim of this study is to overview the etiology and symptoms of these clinical conditions; furthermore to offer technical proposals for the required diagnostic and therapeutical steps via case reports. Furthermore, hepatic injury, caused by ischemia-reperfusion secondary to total vascular occlusion (Pringle maneuver) used in hepatic surgery is outlined. Orv. Hetil., 2015, 156(48), 1938–1948.

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24

Jourabchi, Natanel, Justin Pryce McWilliams, Edward Wolfgang Lee, Steven Sauk, and Stephen Thomas Kee. "TIPS Placement via Combined Transjugular and Transhepatic Approach for Cavernous Portal Vein Occlusion: Targeted Approach." Case Reports in Radiology 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/635391.

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Purpose. We report a novel technique which aided recanalization of an occluded portal vein for transjugular intrahepatic portosystemic shunt (TIPS) creation in a patient with symptomatic portal vein thrombosis with cavernous transformation. Some have previously considered cavernous transformation a contraindication to TIPS.Case Presentation. 62-year-old man with chronic pancreatitis, portal vein thrombosis, portal hypertension and recurrent variceal bleeding presents with melena and hematemesis. The patient was severely anemic, hemodynamically unstable, and required emergent portal decompression. Attempts to recanalize the main portal vein using traditional transjugular access were unsuccessful. After percutaneous transhepatic right portal vein access and navigation of a wire through the occluded main portal vein, an angioplasty balloon was inflated at the desired site of shunt takeoff. The balloon was targeted and punctured from the transjugular approach, and a wire was passed into the portal system. TIPS placement then proceeded routinely.Conclusion. Although occlusion of the portal vein increases difficulty of performing TIPS, it should not be considered an absolute contraindication. We have described a method for recanalizing an occluded portal vein using a combined transhepatic and transjugular approach for TIPS. This approach may be useful to relieve portal hypertension in patients who fail endoscopic and/or surgical therapies.

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25

Ausania, F., R. Jackson, T. Tsirlis, and RM Charnley. "Portal vein occlusion following pancreatico-duodenectomy and portal vein resection: treatment by percutaneous portal vein stent." Annals of The Royal College of Surgeons of England 95, no. 4 (May 1, 2013): 299. http://dx.doi.org/10.1308/003588413x13629960046075c.

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26

Hamza, Shereen M., and Susan Kaufman. "Effect of mesenteric vascular congestion on reflex control of renal blood flow." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 5 (November 2007): R1917—R1922. http://dx.doi.org/10.1152/ajpregu.00180.2007.

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Portal hypertension initiates a splenorenal reflex, whereby increases in splenic afferent nerve activity and renal sympathetic nerve activity cause a decrease in renal blood flow (RBF). We postulated that mesenteric vascular congestion similarly compromises renal function through an intestinal-renal reflex. The portal vein was partially occluded in anesthetized rats, either rostral or caudal to the junction with the splenic vein. Portal venous pressure increased (6.5 ± 0.1 to 13.2 ± 0.1 mmHg; n = 78) and mesenteric venous outflow was equally obstructed in both cases. However, only rostral occlusion increased splenic venous pressure. Rostral occlusion caused a fall in RBF (−1.2 ± 0.2 ml/min; n = 9) that was attenuated by renal denervation (−0.5 ± 0.1 ml/min; n = 6), splenic denervation (−0.2 ± 0.1 ml/min; n = 11), celiac ganglionectomy (−0.3 ± 0.1 ml/min; n = 9), and splenectomy (−0.5 ± 0.1 ml/min; n = 6). Caudal occlusion induced a significantly smaller fall in RBF (−0.5 ± 0.1 ml/min; n = 9), which was not influenced by renal denervation (−0.2 ± 0.2 ml/min; n = 6), splenic denervation (−0.1 ± 0.1 ml/min; n = 7), celiac ganglionectomy (−0.1 ± 0.3 ml/min; n = 8), or splenectomy (−0.3 ± 0.1 ml/min; n = 7). Renal arterial conductance fell only in intact animals subjected to rostral occlusion (−0.007 ± 0.002 ml·min−1·mmHg−1). This was accompanied by increases in splenic afferent nerve activity (15.0 ± 3.5 to 32.6 ± 6.2 spikes/s; n = 7) and renal efferent nerve activity (32.7 ± 5.2 to 39.3 ± 6.0 spikes/s; n = 10). In animals subjected to caudal occlusion, there were no such changes in renal arterial conductance or splenic afferent/renal sympathetic nerve activity. We conclude that the portal hypertension-induced fall in RBF is initiated by increased splenic, but not mesenteric, venous pressure, i.e., we did not find evidence for intestinal-renal reflex control of the kidneys.

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27

Dou, Lei, Wei-Shan Meng, Bao-Dong Su, Peng Zhu, Wei Zhang, Hui-Fang Liang, Yi-Fa Chen, and Xiao-Ping Chen. "Step-by-step Vascular Control for Extracapsular Resection of Complex Giant Liver Hemangioma Involving the Inferior Vena Cava." American Surgeon 80, no. 1 (January 2014): 15–20. http://dx.doi.org/10.1177/000313481408000111.

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Massive hemorrhage remains an important clinical problem in extracapsular resection of giant liver hemangiomas (GLHs), especially for those involving the proximal hepatic veins and/or inferior vena cava. Between July 2004 and March 2012, 87 patients with a complex GLH scheduled for surgical treatment were included in this study. All patients were underwent vascular preparation (Step 1), advanced hepatic artery clamping (Step 2), and stepwise vascular occlusion (Step 3). Intraoperative blood loss, blood transfusion volume, degree of ischemia–reperfusion injury, and postoperative complications were recorded. No patients required urgent vascular preparation to manage intraoperative bleeding. In total, 87, 64, and 21 patients had portal triad (PT), infra-hepatic inferior vena cava (IVC), and suprahepatic IVC preparation; and 17, 43, and 11 patients had PT, PTand suprahepatic IVC, and all three (PT, infra-, and suprahepatic IVC) occlusions. The PT, infrahepatic IVC, and SIVC occlusion times were 12.1 ± 3.7 minutes, 7.9 ± 2.4 minutes, and 3.2 ± 1.4 minutes, respectively. Mean blood loss was 291.9 ± 124.5 mL, and only four patients received blood transfusions. No patients had life-threatening complications or died (Clavien-Dindo Grade 4, 5). Compared with paralleled studies, this technique has an advantage to decrease the blood loss in less liver ischemia time. For complex GLH resections, the described step-by-step vascular control technique was efficacious and feasible for controlling intraoperative bleeding.

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28

Garbuzov, Roman V., Yu A. Polyaev, A. E. Stepanov, and A. A. Mylnikov. "ABERNATHY MALFORMATIONS IN CHILDREN. EXPERIENCE IN ENDOVASCULAR AND SURGICAL TREATMENT." Russian Journal of Pediatric Surgery 24, no. 2 (May 12, 2020): 71–77. http://dx.doi.org/10.18821/1560-9510-2020-24-2-71-77.

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Introduction. Congenital portosystemic shunt (SPSS) is a congenital anomaly of the portal system. Blood from the portal system, bypassing the hepatic bloodstream, enters the systemic venous bloodflow. Clinical manifestations are not specific. SPSS can be suspected in patients with arterial hypoxemia and intrapulmonary vascular dilatation, in patients with foci of nodular hyperplasia in the liver, with carbohydrate metabolism disorders in the form of hyperinsulinemia and hypoglycemia, hepatic encephalopathy, hyperammoniemia. Material and methods. Nine patients ( five boys and four girls) , aged 7.7 ± 5.2, were treated in our clinic. All patients had hyperammonemia before surgery 124.5 ± 24.7 μmol / L. Five patients had endovascular SPSS occlusion. Four patients had open SPSS ligation. Results. An immediate technical success was achieved in all patients. There were no complications after endovascular treatment. There was one relapse which required a repeated endovascular occlusion. After endovascular occlusion, the length of hospital stay was shorter, postoperative period was much easier; there were no serious complications compared with the open SPSS ligation. Blood ammonia returned to normal levels in eight patients. In one patient who had multiple shunts and incomplete occlusion, blood ammonia level decreased by twice, up to 82 μmol / L. Conclusion. If SPSS is revealed, a surgical intervention is recommended to separate the portal and systemic venous blood flow. In the surgical treatment for SPSS, X-ray surgical endovascular occlusion is more preferable. If this technique was not possible, surgeons performed open surgical intervention.

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Citron, S. J., S. A. Cohen, S. D. Brantley, and W. A. Troyer. "PERCUTANEOUS SPLENIC ACCESS TO RELIEVE PORTAL VENOUS OCCLUSION." Journal of Pediatric Gastroenterology &amp Nutrition 25, no. 4 (October 1997): 478. http://dx.doi.org/10.1097/00005176-199710000-00161.

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Oka, Tatsuhiro, Tetsuro Ohwada, Tadanobu Mizuguchi, and Akira Kochi. "Effects of portal vein occlusion on myocardial contractility." Journal of Anesthesia 5, no. 4 (October 1991): 344–51. http://dx.doi.org/10.1007/s0054010050344.

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Hasegawa, Takaaki, Koichiro Yamakado, Haruyuki Takaki, Atsuhiro Nakatsuka, Junji Uraki, Takashi Yamanaka, Masashi Fujimori, Shugo Mizuno, Shuji Isaji, and Hajime Sakuma. "Portal Venous Stent Placement for Malignant Portal Venous Stenosis or Occlusion: Who Benefits?" CardioVascular and Interventional Radiology 38, no. 6 (May 20, 2015): 1515–22. http://dx.doi.org/10.1007/s00270-015-1123-2.

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Li, Bin, Yan Zhu, Lei Xie, Shuyang Hu, Shupeng Liu, and Xiaoqing Jiang. "Portal vein ligation alters coding and noncoding gene expression in rat livers." Biochemistry and Cell Biology 96, no. 1 (February 2018): 1–10. http://dx.doi.org/10.1139/bcb-2017-0070.

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Portal vein occlusion increases the resectability of initially unresectable liver cancer by inducing hypertrophy in non-occluded liver lobes. However, the mechanisms of how portal vein occlusion induces hepatic hypertrophy remain unclear. A cDNA microarray was used to identify the gene expression signatures of ligated (LLLs) and nonligated liver lobes (NLLLs) at different time points after portal vein ligation (PVL). The results of a bioinformatics analysis revealed that LLLs and NLLLs displayed different gene expression profiles. Moreover, the expression levels of both coding and noncoding RNA were different between LLLs and NLLLs at different time points after PVL. A series test of cluster analysis revealed that the No. 22 and No. 5 expression patterns, which showed altered expression at 24 h and maintained this altered expression over the following 14 days, had the lowest P values and the highest number of differentially expressed genes in both the LLLs and NLLLs. The results of a GO analysis showed the activation of hypoxia pathways in LLLs and the activation of cell proliferation and cell-cycle pathways in NLLLs, suggesting the involvement of these pathways in PVL-induced hepatic hypertrophy and regeneration. These results provide insight into the molecular mechanisms underlying hepatic hypertrophy and regeneration induced by portal vein occlusion, and they identify potential targeting pathways that can promote the clinical application of PVL in liver cancer therapy.

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Dias, Miguel Angel, Reginaldo Ceneviva, Jorge Elias Jr., Sergio Zucoloto, Caroline Floreoto Baldo, and Paulo Roberto Barbosa Évora. "Liver histological, portal flow and plasmatic nitric oxide alterations caused by biliary obstruction and drainage in rats." Acta Cirurgica Brasileira 23, suppl 1 (2008): 2–7. http://dx.doi.org/10.1590/s0102-86502008000700002.

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PURPOSE: To evaluate liver alterations caused by biliary obstruction and drainage. METHODS: Thirty-nine male Wistar rats were randomly distributed in 4 groups: BO (n=18) bile duct ligation for 20 days, with a periodic evaluation of liver histological alterations, Doppler echography portal flow and measurements of NO and malondialdehyde (MDA); BO/DB (n=13) bile duct occlusion for 20 days followed by biliary drainage by choledochoduodenal anastomosis, 5 days follow-up, same BO group parameters evaluations; group CED (n=4) sham operation and portal flow evaluation trough 20 days; CHB (n=4) sham operation, with hepatic biopsy on 25th day and followed-up trough 25 days, by the same parameters of group BO, with exception of portal flow. Direct bilirubin (DB) and alkaline phosphatase (AP) were evaluated in the group BO, BO/DB and CHB. RESULTS: The bile duct ligation led to an increase of DB and AP, development of liver histological alterations, reduction of portal flow and increase of plasmatic NO and of MDA levels. The bile duct clearing resulted in a reduction of DB, AP, NO, MDA histological alterations and increase of portal flow. CONCLUSION: The biliary occlusion resulted in cholestasis and portal flow reduction, besides the increase of plasmatic NO and of hepatic MDA levels, and histological liver alterations, with a tendency of normalization after the bile duct clearing.

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34

Mountfort, Katrina, Mohamad Mohty, and Elisabeth Wallhult. "Defibrotide – A New Treatment Approach for Severe Veno-occlusive Disease." European Oncology & Haematology 11, no. 1 (2015): 11. http://dx.doi.org/10.17925/eoh.2015.11.01.11.

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Severe veno-occlusive disease (VOD) is a serious and life-threatening complication of haematopoietic stem cell transplantation (HSCT), for which the standard of care has until recently been supportive care. VOD is the result of a primary injury to sinusoidal endothelial cells and severe VOD is characterised by sinusoidal narrowing and occlusion, which leads to portal hypertension, multi-organ failure (MOF) and, ultimately, death. Defibrotide regulates multiple pathways involved in the pathological processes underlying VOD and is the first drug to be approved in Europe for the treatment of severe VOD. Defibrotide is indicated for the treatment of severe hepatic VOD in HSCT therapy in adults and infants aged over 1 month. A phase III study found significant increases in complete response (CR) and survival with defibrotide compared with historical controls. These data together with earlier studies and an ongoing expanded access protocol in a large patient cohort demonstrate improved outcomes with defibrotide in severe VOD and highlight the importance of treatment with defibrotide

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35

Jaffe, V., B. Alexander, and R. T. Mathie. "Intrahepatic portal occlusion by microspheres: a new model of portal hypertension in the rat." Gut 35, no. 6 (June 1, 1994): 815–18. http://dx.doi.org/10.1136/gut.35.6.815.

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36

Kameoka, Nobuhisa, Kazuo Chijiiwa, Shyuji Saiki, and Masao Tanaka. "Advantage of preoperative portal vein occlusion for hepatectomy that exceeds portal vein occluded lobes." Surgery 123, no. 5 (May 1998): 545–53. http://dx.doi.org/10.1067/msy.1998.86985.

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37

Shibamoto, T., H. G. Wang, S. Tanaka, and S. Koyama. "Hepatic capillary pressure is estimated using triple vascular occlusion method in isolated canine liver." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 5 (November 1, 1996): R1130—R1141. http://dx.doi.org/10.1152/ajpregu.1996.271.5.r1130.

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We determined whether the triple vascular occlusion pressure (Pto), the equilibration pressure obtained when the hepatic artery, portal, and hepatic veins were occluded simultaneously, represented the capillary pressure (Pc) in isolated bivascularly blood-perfused canine livers. Effects of a bolus injection of histamine (0.1-60 micrograms), norepinephrine (NE; 1-600 micrograms), or acetylcholine (ACh; 0.01-10 micrograms) into the portal vein or the hepatic artery were also studied on vascular resistance distribution using Pto as a measure of Pc. The livers were perfused at constant flow via the portal vein and at constant pressure via the hepatic artery. Pto was compared with Pc measured using the traditional gravimetric method (Pc,i). Pto and Pc,i showed a strong correlation (Pto = -0.02 + 0.98 Pc,i; r = 0.83, P = 0.0018). With comparisons, the intercept was not significantly different from zero, and the slope was not different from 1.00, indicating that Pto accurately represented Pc. The resting postsinusoidal vascular resistance comprised 54% of the total hepatic vascular resistance (Rt). Portal or arterial injection of histamine increased predominantly hepatic venous resistance (Rhv) over portal resistance with liver weight gain. NE constricted both the portal vein and the hepatic artery in greater magnitude than the hepatic vein, as evidenced by a significant decrease in the Rhv/Rt ratio. This precapillary constriction was accompanied by a significant decrease in liver weight. In contrast, ACh contracted both portal and hepatic veins similarly without liver weight change. We conclude that Pto is an excellent estimate of Pc in isolated blood-perfused canine livers and that the hepatic vascular resistance sites in the resting states are located evenly in the pre- and postsinusoidal vessels. Intraportal or intra-arterial infusion of histamine, NE, and ACh produced characteristically different changes in hepatic vascular resistances and hepatic volume. The Pto technique could be applied in experimental research on hepatic hemodynamics.

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Cohen, Ronny, Thierry Mallet, Michael Gale, Remigiusz Soltys, and Pablo Loarte. "Portal Vein Thrombosis." Case Reports in Vascular Medicine 2015 (2015): 1–5. http://dx.doi.org/10.1155/2015/823063.

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Portal vein thrombosis (PVT) is the blockage or narrowing of the portal vein by a thrombus. It is relatively rare and has been linked with the presence of an underlying liver disease or prothrombotic disorders. We present a case of a young male who presented with vague abdominal symptoms for approximately one week. Imaging revealed the presence of multiple nonocclusive thrombi involving the right portal vein, the splenic vein, and the left renal vein, as well as complete occlusion of the left portal vein and the superior mesenteric vein. We discuss pathogenesis, clinical presentation, and management of both acute and chronic thrombosis. The presence of PVT should be considered as a clue for prothrombotic disorders, liver disease, and other local and general factors that must be carefully investigated. It is hoped that this case report will help increase awareness of the complexity associated with portal vein thrombosis among the medical community.

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39

Rajeswaran, Shankar, and Victoria Young. "Management of Portal Hypertension in the Pediatric Population: A Primer for the Interventional Radiologist." Seminars in Interventional Radiology 35, no. 03 (August 2018): 160–64. http://dx.doi.org/10.1055/s-0038-1660794.

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AbstractInterventional radiology's role in the management of portal hypertension in the pediatric population differs from the management of adult portal hypertension. In the pediatric population, portal hypertension is frequently secondary to thrombosis and cavernous transformation of the extrahepatic portion of the portal vein. Transjugular intrahepatic portosystemic shunt can be utilized to manage portal hypertension in children with intrinsic liver disease that results in cirrhosis and portal hypertension, and is often used as a bridge to transplant. While technically feasible in extrahepatic portal vein occlusion, the sequelae of portosystemic shunting are less desirable in a child. The Meso-Rex bypass procedure, which represents the mainstay of management for pediatric portal hypertension, provides surgical relief of extrahepatic portal vein obstruction and restores mesenteric venous blood flow to the liver. This article aims to review management of portal hypertension in children as it pertains to the interventional radiologist, including preoperative assessment, postoperative evaluation, and the management of complications of the Meso-Rex bypass.

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Yu, S. C. H., and K. J. Cho. "Carbon dioxide wedged arterial splenoportography: A new technique—a case report and an experimental study." Acta Radiologica 50, no. 3 (April 2009): 265–69. http://dx.doi.org/10.1080/02841850802712676.

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Background: Patients with splenic vein occlusion may present a diagnostic problem when the location, morphology, and cause of the obstructive lesion and the associated collateral veins cannot be clearly defined by standard diagnostic imaging modalities such as computed tomography, magnetic resonance venography, or indirect splenoportography (arterial portography). Purpose: To evaluate the safety and effectiveness of carbon dioxide (CO2) wedged arterial splenoportography for definitive investigation of splenic vein occlusion. Material and Methods: Following unsuccessful diagnosis with computed tomography and standard contrast arterial portography in a patient with recurrent gastric variceal bleeding, CO2 was injected into a wedged splenic arterial catheter and successfully outlined splenic vein occlusion and gastric varices. Our experience with this patient prompted us to perform an experimental study in swine to evaluate the safety and effectiveness of CO2 wedged arterial splenoportography for visualization of the splenic and portal veins. A microcatheter was advanced coaxially and wedged into the splenic arteries of three pigs. After checking the wedged positioning with contrast medium injection, CO2 was injected manually and the splenic region imaged. The spleens were then removed for gross and microscopic examinations. Results: In the patient, CO2 wedged arterial splenoportography demonstrated gastric varices associated with splenic vein occlusion. In all animals, CO2 wedged arterial splenoportography visualized the splenic and portal veins. No CO2 extravasations occurred in the spleen. Gross and microscopic examinations revealed no evidence of splenic rupture or intrasplenic hematoma. Conclusion: CO2 wedged arterial splenoportography may be a useful method for visualizing gastric varices associated with splenic vein occlusion. This new technique has the potential to replace the standard splenic arterial portography for visualization of splenic and portal veins, thus eliminating the need for injection of a large volume of iodinated contrast material. Further clinical studies are justified to evaluate this technique.

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Wang, Jianfeng, Weili Yang, Qiang Huang, Kun Gao, Baojie Wei, Renyou Zhai, and Yaoping Shi. "Interventional Treatment for Portal Venous Occlusion After Liver Transplantation." Medicine 94, no. 4 (January 2015): e356. http://dx.doi.org/10.1097/md.0000000000000356.

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42

Liu, Jiacheng, Chen Zhou, Qin Shi, Jinqiang Ma, Tianhe Ye, Chuansheng Zheng, Gansheng Feng, and Bin Xiong. "Exploration of interventional therapy strategy for portal vein occlusion." European Journal of Gastroenterology & Hepatology 32, no. 4 (April 2020): 507–16. http://dx.doi.org/10.1097/meg.0000000000001586.

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43

Herrero, Astrid, Regis Souche, Fabrizio Panaro, and Francis Navarro. "Endovascular balloon occlusion during reconstruction of portal vein injury." Langenbeck's Archives of Surgery 405, no. 3 (May 2020): 391–95. http://dx.doi.org/10.1007/s00423-020-01886-z.

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44

Chijiiwa, Kazuo. "Functional Contribution of Preoperative Portal Vein Occlusion to Hepatectomy." Archives of Surgery 131, no. 7 (July 1, 1996): 779. http://dx.doi.org/10.1001/archsurg.1996.01430190101025.

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45

Stringer, M. D., N. D. Heaton, J. Karani, S. Olliff, and E. R. Howard. "Patterns of portal vein occlusion and their aetiological significance." British Journal of Surgery 81, no. 9 (September 1994): 1328–31. http://dx.doi.org/10.1002/bjs.1800810923.

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46

Knezevic, Mario, Slaven Gojkovic, Ivan Krezic, Helena Zizek, Dominik Malekinusic, Borna Vrdoljak, Hrvoje Vranes, et al. "Occlusion of the Superior Mesenteric Artery in Rats Reversed by Collateral Pathways Activation: Gastric Pentadecapeptide BPC 157 Therapy Counteracts Multiple Organ Dysfunction Syndrome; Intracranial, Portal, and Caval Hypertension; and Aortal Hypotension." Biomedicines 9, no. 6 (May 26, 2021): 609. http://dx.doi.org/10.3390/biomedicines9060609.

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Gastric pentadecapeptide BPC 157 therapy counteracts multiple organ dysfunction syndrome in rats, which have permanent occlusion of the superior mesenteric artery close to the abdominal aorta. Previously, when confronted with major vessel occlusion, its effect would rapidly activate collateral vessel pathways and resolve major venous occlusion syndromes (Pringle maneuver ischemia, reperfusion, Budd–Chiari syndrome) in rats. This would overwhelm superior mesenteric artery permanent occlusion, and result in local, peripheral, and central disturbances. Methods: Assessments, for 30 min (gross recording, angiography, ECG, pressure, microscopy, biochemistry, and oxidative stress), included the portal hypertension, caval hypertension, and aortal hypotension, and centrally, the superior sagittal sinus hypertension; systemic arterial and venous thrombosis; ECG disturbances; MDA-tissue increase; and multiple organ lesions and disturbances, including the heart, lung, liver, kidney, and gastrointestinal tract, in particular, as well as brain (cortex (cerebral, cerebellar), hypothalamus/thalamus, hippocampus). BPC 157 therapy (/kg, abdominal bath) (10 µg, 10 ng) was given for a 1-min ligation time. Results: BPC 157 rapidly recruits collateral vessels (inferior anterior pancreaticoduodenal artery and inferior mesenteric artery) that circumvent occlusion and ascertains blood flow distant from the occlusion in the superior mesenteric artery. Portal and caval hypertension, aortal hypotension, and, centrally, superior sagittal sinus hypertension were attenuated or eliminated, and ECG disturbances markedly mitigated. BPC 157 therapy almost annihilated venous and arterial thrombosis. Multiple organ lesions and disturbances (i.e., heart, lung, liver, and gastrointestinal tract, in particular, as well as brain) were largely attenuated. Conclusions: Rats with superior mesenteric artery occlusion may additionally undergo BPC 157 therapy as full counteraction of vascular occlusion-induced multiple organ dysfunction syndrome.

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Hillaire, S., D. Cazals-Hatem, M. Rudler, A. Plessier, C. Francoz, F. Durand, P. Bedossa, and D. Valla. "P.147 Veinopathie portale occlusive : étude rétrospective de 59 patients." Gastroentérologie Clinique et Biologique 33, no. 3 (March 2009): A92. http://dx.doi.org/10.1016/s0399-8320(09)72778-2.

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48

Caldwell, W. M., D. P. McKown, J. A. Bleck, J. W. Hartley, T. Erdal, E. E. Barrett, and D. Franklin. "An automatic syringe for coronary occlusion in long-term collateralization studies." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 6 (June 1, 1989): H1707—H1710. http://dx.doi.org/10.1152/ajpheart.1989.256.6.h1707.

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A portable apparatus for performing repeated, brief coronary artery occlusions automatically in long-term chronic studies involving dogs and larger animals is described. The battery-operated, back-pack-carried device uses a motorized syringe driven by a digital-programmable timing circuit to inflate a coronary artery occluder for durations of 10 s to 3 min at intervals from 14 s to 16 h. A single battery charge produces 450 occlusions. The generated pressure is adjustable to 1,000 mmHg maximum. A separate fail-safe circuit monitors system operation to open a pressure-relief valve if occlusions exceed a preset duration.

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Hulshoff, Jan Binne, Frans J. C. Cuperus, and Robbert J. de Haas. "Mass-Forming Portal Biliopathy Presenting as Extreme Wall-Thickening of the Common Bile Duct." Diagnostics 10, no. 9 (August 22, 2020): 623. http://dx.doi.org/10.3390/diagnostics10090623.

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Portal biliopathy refers to biliary tree abnormalities in patients with peribiliary collateral vessels and non-neoplastic extrahepatic portal vein occlusion. These biliary abnormalities are caused by vascular compression and ischemic damage of the biliary tree, which can result in bile duct compression, stenosis, fibrotic strictures, bile duct dilation, and thickening of the bile duct wall. Portal biliopathy is difficult to distinguish from cholangiocarcinoma, IgG4-related disease, and sclerosing cholangitis. Although most patients are asymptomatic, portal biliopathy can lead to serious complications, such as recurrent cholangitis. This case illustrates the importance of including portal biliopathy in the differential diagnosis at an early stage, especially in patients with portal hypertension. With early recognition, the need for additional invasive diagnostic procedures such as biopsies is minimized. Pathogenesis, clinical presentation, diagnostics, and treatment options of portal biliopathy are described in the article.

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Swersky, Adam, and Prasoon P. Mohan. "Simultaneous Transjugular Intrahepatic Portosystemic Shunt Revision and Embolization of an Arterioportal Fistula in a Patient with Active Variceal Bleeding from Systemic Lupus Erythematosus-induced Cirrhosis." American Journal of Interventional Radiology 4 (April 18, 2020): 3. http://dx.doi.org/10.25259/ajir_12_2019.

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Transjugular intrahepatic portosystemic shunt (TIPS) occlusion is a common occurrence that can be managed based on the nature and acuity of shunt failure. Arterioportal fistulas (APFs) are rare communications between portal venous and systemic arterial vasculature that can present with symptomatic portal hypertension. In this case, we describe the management of a patient with variceal bleeding due to TIPS dysfunction complicated by the presence of an APF.

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