Superior Mesenteric Arterial Portography Research Articles

Portal vein embolization following arterial portography for the management of an active portal bleeding after blunt liver trauma in a cirrhotic patient

BackgroundThe management of blunt liver trauma in cirrhotic patients is challenging, because while bleeding is most often of arterial origin, the increased pressure in the portal system associated with cirrhosis can increase the risk of portal bleeding, which is sometimes difficult to confirm on contrast-enhanced abdominal computed tomography.Case presentationWe managed a 54-year-old cirrhotic patient who presented with blunt liver trauma. Computed Tomography showed active intraperitoneal bleeding presumed to be of hepatic origin. Given the patient's hemodynamic stability, the decision was made to manage the patient non-surgically. The patient underwent hepatic arteriography to rule out an arterial origin to the bleeding. A superior mesenteric arterial portography confirmed the portal venous origin of the bleeding. To stop the bleeding, a distal portal vein embolization using coils and glue was performed by approaching a large paraumbilical vein.ConclusionsOur case study shows the value of arterial portography in the management of these patients, when they are clinically stable enough to benefit from non-surgical management; This allows arterial bleeding to be excluded on hepatic arteriography, portal bleeding to be confirmed on portography following arteriography in the superior mesenteric artery, and guidance of portal vein embolization.

Transjugular Retrograde Obliteration prior to Liver Resection for Hepatocellular Carcinoma Associated with Hyperammonemia due to Spontaneous Portosystemic Shunt.

A 67-year-old woman had hepatocellular carcinoma (HCC) measuring 3.7 cm at S8 of the liver with hyperammonemia due to a spontaneous giant mesocaval shunt. Admission laboratory data revealed albumin, 2.9 g/dL; total bilirubin, 1.3 mg/dL; plasma ammonia level (NH3), 152 g/dL; total bile acid (TBA) 108.5 μmoL/L; indocyanine green retention rate at 15 min (ICG15), 63%. Superior mesenteric arterial portography revealed a hepatofugal giant mesocaval shunt, and the portal vein was not visualized. Before surgery, transjugular retrograde obliteration (TJO) for the mesocaval shunt was attempted to normalize the portal blood flow. Via the right internal jugular vein, a 6 F occlusive balloon catheter was inserted superselectively into the mesocaval shunt. The mesocaval shunt was successfully embolized using absolute ethanol and a 50% glucose solution. Eleven days after TJO, NH3, TBA, and ICG15 decreased to 56, 44, and 33, respectively. Superior mesenteric arterial portography after TJO revealed a hepatopetal portal flow. Partial hepatectomy of S8 was performed 25 days after TJO. The subsequent clinical course showed no complications, and the woman was discharged on postoperative day 14. We conclude that the combined therapy of surgery and TJO is an effective means of treating HCC with hyperammonemia due to a spontaneous portosystemic shunt.

Percutaneous transretroperitoneal direct approach to occlude a major shunt in a patient with extrahepatic portal–systemic encephalopathy

A 73-year-old woman had sudden dystrophy and amnesia in our hospital. Her serum ammonia level was high. Marked collateral vessels from the splenic vein to the left renal vein around the spleen were seen on a computed tomography (CT) scan with contrast enhancement. An abdominal angiogram showed that the direction of the splenic vein was hepatofugal on superior mesenteric arterial portography, with a marked splenorenal shunt on splenic arterial portography. Hepatic encephalopathy due to a marked extrahepatic portal-systemic shunt was diagnosed. Transjugular retrograde obliteration (TJO) was attempted, but the catheter and guide wire could not selectively approach the splenorenal shunt because of many outflow routes. We punctured the vessels from the left side of the back under ultrasonographic guidance. We injected microcoils and ethanolamine oleate to completely obliterate the shunt. Marked collateral vessels showed no venous flow on a CT scan after treatment. The serum ammonia level was in the normal range. There has been no recanalization of the shunt vessels for 4 years after treatment. Hepatic encephalopathy has not recurred, and no other collateral vessels have developed. To our knowledge, this is the first report to document the use of a percutaneous transretroperitoneal direct approach to occlude a major shunt in a patient with extrahepatic portal-systemic encephalopathy.

Computed tomography perfusion of the liver: assessment of pure portal blood flow studied with CT perfusion during superior mesenteric arterial portography

To quantitatively assess the portal component of hepatic blood flow using computed tomography (CT) perfusion studies during superior mesenteric arterial portography. Thirty-four patients with hepatocellular carcinoma and liver cirrhosis (LC) and 13 patients with liver metastasis without chronic liver disease were enrolled in this study. Ten milliliters of a non-ionic contrast medium (150 mg I) was injected at a rate of 5 ml/s via a catheter placed in the superior mesenteric artery. Single-slice cine CT images at the level of the main trunk or the right/left main trunk of the portal vein were acquired over 40 s. The deconvolution method was then used on these CT images to measure blood flow (BF), blood volume (BV), and mean transit time (MTT) in (a) liver parenchyma in patients with HCC and liver cirrhosis; (b) liver parenchyma in patients with liver metastasis without cirrhosis; (c) directly in the HCC; and (d) directly in one of the metastases. In 34 LC patients (a), BF, BV, and MTT in the liver parenchyma were 44.7+/-24.5 ml/min/100 g, 3.9+/-2.4 ml/100 g, and 10.9+/-5.5 s, respectively. In 13 patients without cirrhosis (b), BF, BV, and MTT in the liver parenchyma were 89.6+/-52.0 ml/min/100 g, 6.3+/-3.2 ml/100 g, and 8.7+/-3.6 sec, respectively. A significant difference in BF and BV was seen in patients with liver cirrhosis compared to those without cirrhosis. BF, BV, and MTT measured directly in HCC (c) were 6.5+/-4.5 ml/min/100 g, 0.4+/-0.4 ml/100 g, and 3.0+/-3.1 sec respectively, and BF, BV, and MTT in liver metastases (d) were 19.3+/-21.7 ml/min/100 g, 0.6+/-0.8 ml/100 g, and 1.8+/-1.6 s, respectively. CT perfusion studies during superior mesenteric arterial portography allow quantitative assessment of pure portal blood flow in the liver.

Reversal of Portosystemic Encephalopathy after Endoscopic Embolization of Recurrent Gastroesophageal Varices

Abstract:Chronic portosystemic encephalopathy (CPSE) due to a shunt via gastroesophageal varices is uncommon. We were able to control a case of CPSE due to recurrent gastroesophageal varices using endoscopic embolization (EE). A 68‐year‐old man presented at our hospital in a confused, apathetic and tremulous state. He had undergone devascularization, proximal gastric transection and splenectomy for esopha‐geal varices due to liver cirrhosis 16 years previously. The patient had hyperammone‐mia (228 µg/dl), and endoscopic examination revealed nodular cardiac varices and large recurrent esophageal varices. Superior mesenteric arterial portography revealed that a large volume of superior mesenteric venous blood drained into the cardiac and esophageal varices through the remnant left gastric vein. The plasma ammonia level in the esophageal varices taken at the time of EE was 419 pg/dl, which was a much higher level than that of peripheral vessels, the superior vena cava and azygos vein, and suggested that the encephalopathy was due to the portosystemic shunt via the gastroesophageal varices. EE was performed using 5% ethanolamine oleate with iopamidol under fluoroscopy. The esophageal and cardiac varices were successfully embolized, the CPSE disappeared, and the plasma ammonia level decreased to 27 pg/dl. No complications were observed, and the patient was discharged on day 37 after EE. We conclude that EE is an effective and safe treatment for CPSE due to gastroesophageal varices.

Chronic rejection following primary adult liver transplantation under tacrolimus: [formula omitted]. Pittsburgh Transplantation Institute, University of Pittsburgh, Pittsburgh, PA

A portal hemodynamic study was made in 7 consecutive patients with chronic portal-systemic encephalopathy by percutaneous transhepatic catheterization of the portal vein and injecting contrast medium into the superior mesenteric vein or by superior mesenteric arterial portography in comparison with patients without encephalopathy studied by percutaneous catheterization of these veins. All 7 patients had a large gastro-renal or spleno-renal shunt, and a large proportion of superior mesenteric venous blood was being shunted as estimated from the diameter of the portal and the collateral vein, whereas in nonencephalopathic patients in whom part of the superior mesenteric venous blood was shunting this diversion was much less (P < 0.001). Only one of the chronic portal-systemic encephalopathic patients had esophageal varices, insignificant in size, and the incidence of esophageal varices was significantly less compared to the 12 nonencephalopathic control patients with portal hypertension who had either a gastro-renal or spleno-renal shunt (P < 0.05). It is suggested that chronic portal-systemic encephalopathy is a result of a large collateral route shunting a large proportion of the superior mesenteric venous blood into systemic circulation, and that development of such collaterals precludes formation of large esophageal varices.

False-positive CT portography: correlation with pathologic findings.

A retrospective study was performed to determine the causes of false-positive diagnoses based on CT findings obtained during superior mesenteric arterial portography (CT portography) and to correlate the imaging characteristics of the incorrectly diagnosed lesions with their pathologic findings. In a series of 52 patients who had CT portography before surgical exploration of the liver, eight had a total of 10 false-positive findings, yielding a false-positive diagnosis rate of 15%. In eight cases, the false-positive findings from CT portography were correlated with the histologic material obtained during partial hepatic resection or intraoperative biopsies at the corresponding sites. Of the 10 false-positive findings on CT portograms, seven led to false-positive diagnoses of hepatic tumors. Conversely, three nontumorous false-positive findings were erroneously considered to be portal perfusion defects. The final diagnoses based on pathologic findings included focal fatty infiltration of the liver (three), cirrhosis (two), and portal perfusion defect (three). Two false-positive findings for which no histologic correlation was possible were considered to be portal perfusion defects on the basis of intraoperative findings. Recognition of false-positive findings is crucial in the preoperative evaluation of hepatic tumors because the findings may be interpreted as contraindications for surgery in patients who have operable tumors. The pathologic correlations show that several different entities can cause diagnoses based on CT portographic findings to be false-positive. However, differentiating between those entities remains a diagnostic challenge.

Mesoatrial shunts for Budd-Chiari syndrome and inferior vena cava thrombosis: angiographic and hemodynamic evaluations.

When inferior vena caval obstruction complicates the Budd-Chiari syndrome, conventional portosystemic shunts are not possible. The mesoatrial shunt has been devised to enable portal and sinusoidal decompression in these patients. Findings in 12 patients with Budd-Chiari syndrome and inferior vena caval obstruction in whom a mesoatrial shunt was performed are reported. Preoperative inferior vena cavography with pressure measurements is essential to determine the appropriate shunt procedure. Postoperatively, shunt patency is assessed with superior mesenteric arterial portography. Where possible, transvenous catheterization of the shunt is performed to confirm patency and assess hemodynamic function.

A CASE OF PORTAL-SYSTEMIC ENCEPHALOPATHY

A case of portal-systemic encephalopathy with a large left gastric-left renal shunt is reported. Superior mesenteric arterial portography revealed that a large amount of superior mesenteric venous flow shunted to the inferior vena cava via the left gastric-left renal shunt, and the ratio of the collateral/portal diameter was 2.3. The shunt occlusion test was performed using a balloon catheter in order to investigate the changes in portal circulation after shunt closure. After the occlusion, portal venous pressure rose from 11.0cmH2O to 24.5cmH2O and estimated hepatic blood flow in-creased from 342ml/min/m2 to 923ml/min/m2. Recently, shunt closure surgery has been performed for the treatment of portal-systemic encephalopathy. This report suggested that it would be useful to examine the changes in portal circulation by the shunt occlusion test using a balloon catheter in order to evaluate the effects of this operation preoperatively.

Incidence of portal vein thrombosis in liver cirrhosis: An angiographic study in 708 patients

Portal vein thrombosis was thought to be a common complication of liver cirrhosis in the past. The incidence of angiographically demonstrable portal vein thrombosis was studied in 708 consecutive patients with unequivocal cirrhosis seen in the past 10 yr in whom either transhepatic portography or superior mesenteric arterial portography clearly delineated the major portal vein system. Excluding 2 cases that were thought to be associated with past splenectomy, there were 4 cases of portal vein thrombosis related to cirrhosis, all in a decompensated stage. The calculated incidence of portal vein thrombosis was 0.573% of all cirrhotic patients without splenectomy in the past. They constituted 23.5% of the 17 cases of extrahepatic portal vein obstruction encountered during the same period. There were 78 cases of idiopathic portal hypertension similarly studied angiographically, and the incidence of portal vein thrombosis unrelated to splenectomy was 2.86%. A statistical survey based on 247,728 necropsies recorded in the Japan Autopsy Registries of 1975–1982 showed a 0.05489% incidence of portal vein thrombosis and a 6.58857% incidence of cirrhosis of all types among them, suggesting that portal vein thrombosis is not a common complication of cirrhosis in Japan in recent years.

Portal hemodynamics in chronic portal-systemic encephalopathy: Angiographic study in seven cases

A portal hemodynamic study was made in 7 consecutive patients with chronic portal-systemic encephalopathy by percutaneous transhepatic catheterization of the portal vein and injecting contrast medium into the superior mesenteric vein or by superior mesenteric arterial portography in comparison with patients without encephalopathy studied by percutaneous catheterization of these veins. All 7 patients had a large gastro-renal or spleno-renal shunt, and a large proportion of superior mesenteric venous blood was being shunted as estimated from the diameter of the portal and the collateral vein, whereas in nonencephalopathic patients in whom part of the superior mesenteric venous blood was shunting this diversion was much less (P less than 0.001). Only one of the chronic portal-systemic encephalopathic patients had esophageal varices, insignificant in size, and the incidence of esophageal varices was significantly less compared to the 12 nonencephalopathic control patients with portal hypertension who had either a gastro-renal or spleno-renal shunt (P less than 0.05). It is suggested that chronic portal-systemic encephalopathy is a result of a large collateral route shunting a large proportion of the superior mesenteric venous blood into systemic circulation, and that development of such collaterals precludes formation of large esophageal varices.

Enhanced visualization of the portal vein system in superior mesenteric arterial portography using prostaglandin E1.

The portal vein system was clearly visualized in superior mesenteric arterial portography using prostaglandin E1. Angiographic examination was performed in 68 patients with various liver diseases during the 2 year period from 1980 to 1981. Twenty microgram of prostaglandin E1 was injected into the superior mesenteric artery 30 seconds before injection of 60 ml of contrast medium. The main portal vein was visualized in all of 68 cases. A high rate of success for visualization of the intrahepatic portal vein system by prostaglandin E1 was achieved. The first branches of the intrahepatic portal vein were visualized in 100% of the cases, the second branches in 82%, the third branches in 44%, and the fourth branches in 4% in the right portal vein system. In the left portal vein system, the first branches were visualized in 87%, the second branches in 41%, and the third branches in 3% of the cases. The intrahepatic portal vein system was more clearly visualized in females than in males (P less than 0.05). This procedure is simple, safe and useful for clear visualization of the portal vein system.

Enhanced visualization of the portal system using phentolamine and isoproterenol in combination.

The clinical experience with selective superior mesenteric arterial portography employing an alpha blocking agent (phentolamine) and beta stimulating agent (isoproterenol) used in combination to produce improved portal venous system opacification is described. In fourteen of sixteen studies, a greater degree of opacification of the portal venous system occurred utilizing this drug combination. Various anatomic and physiologic factors, including superior mesenteric artery pressure and peripheral blood pressure before and immediately after the injection of the drug combination were used to evaluate the results. Side effects were minimal and usually consisted of transient tachycardia.