Hepatofugal Blood Flow Research Articles

Management of portal hypertension based on portal hemodynamics.

Portal hypertension is most commonly caused by chronic liver disease. As liver damage progresses, portal pressure gradually elevates and hemodynamics of the portal system gradually change. In normal liver, venous returns from visceral organs join the portal trunk and flow into the liver (hepatopetal blood flow). As portal pressure increases due to liver damage, congestion of some veins of the visceral organ occurs (blood flow to and from). Finally, the direction of some veins (the left gastric vein in particular) of the visceral organ change (hepatofugal blood flow) and develop as collateral veins (portosystemic shunt) to reduce portal pressure. Therefore, esophagogastric varices serve as drainage veins for the portal venous system to reduce the portal pressure. In chronic liver disease, as intrahepatic vascular resistance is increased (backward flow theory) and collateral veins develop, adequate portal hypertension is required to maintain portal flow into the liver through an increase of blood flow into the portal venous system (forward flow theory). Splanchnic and systemic arterial vasodilatations increase the blood flow into the portal venous system (hyperdynamic state) and lead to portal hypertension and collateral formation. Hyperdynamic state, especially around the spleen, is detected in patients with portal hypertension. The spleen is a regulatory organ that maintains portal flow into the liver. In this review, surgical treatment, interventional radiology, endoscopic treatment, and pharmacotherapy for portal hypertension (esophagogastric varices in particular) are described based on the portal hemodynamics using schema.

Hepatofugal Portal Venous Flow: From Normal to Pathological

Whether segmental or diffuse, a hepatofugal blood flow is almost always pathological. Over the years, Doppler ultrasonography has retained its position as one of the most accessible and physiological imaging techniques to evaluate the direction of the portal blood flow. Detection of a reverse flow is important as it may change patient care and outcome.

Left renal vein ligation for large splenorenal shunt during liver transplantation.

Adequate hepatopetal portal vein blood flow is obligatory to ensure proper liver function after liver transplantation. Large collateral veins as shunts impair portal vein flow and even cause hepatofugal blood flow and portal steal syndrome. In particular, splenorenal shunts in liver transplant recipients can lead to allograft dysfunction and possible allograft loss or hepatic encephalopathy. Restoration of portal flow through left renal vein ligation (LRVL) is a treatment option, which is much easier compared to splenectomy, renoportal anastomosis and shunt closure, but bears the risk of moderate and temporary impairment of renal function. In addition, a patent portal vein is mandatory for LRVL. However, although LRVL has been reported to be an effective, safe and easy method to control portacaval shunts and increase hepatopetal flow in some studies, indications and safety are still not clear. In this review, we summarize existing studies on LRVL during liver transplantation.

Quality Improvement Guidelines for Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Portal hypertension is a syndrome caused by increased resistance in the portohepatic circulation and an increase in the splanchnic vein blood supply. In the normal liver, the difference between pressures in the portal vein and the free hepatic veins or right atrium usually does not exceed 5 mm Hg. Portal hypertension is defined as a gradient larger than 6 mm Hg, but clinical complications seem to occur only when the pressure gradient exceeds 10–12 mm Hg. Wedged hepatic pressure measurement has two components. The portal component is the pressure transmitted from the hepatic sinusoids, and the systemic component is the blood pressure transmitted from the central veins. It is the portal component that causes the development of portal systemic collaterals. The term corrected sinusoidal pressure includes only the portal component and is calculated by subtracting the mean right atrial or inferior vena cava pressure from the wedged hepatic venous pressure. Wedged hepatic pressure is obtained through an end-hole catheter that is advanced into a hepatic vein until it can go no further. Alternatively, pressure can be measured through the wire channel of a double lumen balloon catheter inflated in a more central vein. Transjugular intrahepatic portosystemic shunt (TIPS) is the percutaneous method of creating a portosystemic shunt to decrease or treat portal hypertension. TIPS is a side-to-side shunt of a determined diameter designed to function as a partial shunt that preserves a portion of portal flow to the liver [2]. Flow through the completed shunt is assessed by comparing the degree of preferential filling of the shunt to the that of the portal vein branches and portosystemic collaterals (mainly in the gastric veins). The identification of hepatofugal (reversed) blood flow in portal vein branches (total shunting) is a sign of good flow through the shunt. Technical success is defined as a decrease of the portosystemic pressure gradient to 12 mm Hg or less, or a reduction of at least 20 %. Clinical success is defined as cessation of variceal bleeding, decrease of ascites, and conversion into diuretic-sensitive ascites, as well as improvement of liver function in patients referred for massive thrombosis of hepatic veins. Hepatic encephalopathy is defined as the complex of all cerebral dysfunctions that can occur during the course of serious liver disease. Clinical symptomatology, which as a rule is potentially reversible, ranges from disorientation, somnolence, and lethargy to sopor and coma. Hepatic encephalopathy has three forms: type A, associated with acute liver failure; type B, associated with portosystemic bypass without liver disease; and type C, or chronic, associated with liver cirrhosis.

Gastrointestinal: Successful obliteration of bleeding duodenal varices using band ligation

A 57 year old male with hepatitis C and alcohol induced cirrhosis, presented to the emergency with hemetemesis and hematochezia, followed by lightheadness and diaphoresis. He had no history of gastrointestinal hemorrhage. The patient was on warfarin and naproxen following recent knee surgery. He continued to drink 2-3 beers daily. On admission, his BP was 96/60 and pulse was 90/min. Physical exam was otherwise unremarkable. Investigations included a hemoglobin of 7.5 g/dl, platelet count 123, BUN of 30, creatinine 0.7, INR of 1.4 and normal liver enzymes. He was resuscitated with blood and IV fluids, and was started on IV esomeprazole and octreotide. An emergent upper endoscopy demonstrated an oozing duodenal varix between the first and the second portion of the duodenum with a platelet plug (Figure 1). Two bands were successfully placed upon the variceal column (Figure 2). No esophageal or gastric varices were identified. The patient had no further bleeding and was discharged several days later. Follow up endoscopy at one month revealed scarring and healing ulceration at the band ligation sites (Figure 3 arrows). Duodenal varix with platelet plug. Duodenal varix immediately post banding. Duodenal varix site one month later. Varices outside the gastro esophageal region, are referred to as ectopic varices. Ectopic varices are rare, and constitute 1 to 5% of all variceal hemorrhage. Nearly 17% of ectopic variceal bleeding occurs in the duodenum. Duodenal varices (DV) in the absence of esophageal varices, as seen in this patient, are an even more uncommon manifestation of portal hypertension. They result from retroperitoneal porto-systemic shunts caused by increased hepatofugal blood flow through the cystic branch of the superior mesenteric vein, superior and inferior pancreaticoduodenal veins, and gastroduodenal and pyloric veins. Such varices are less effective in lowering the portal pressure, compared with esophageal and gastric varices. The serosal and submucosal location of DV, limits visualization during endoscopy. Their clinical significance is not apparent until the varix expands into the submucosal space where it can hemorrhage into the gastrointestinal lumen. Because of the infrequency of DV hemorrhage, treatment modalities have not been prospectively validated. These include surgical intervention (variceal ligation, duodenal resection, and extra-hepatic portosystemic shunt creation), interventional radiological procedures (tranjugular intrahepatic portosystemic shunt, percutaneous transhepatic obliteration, trans-ileocolic vein obliteration, balloon occluded retrograde transvenous obliteration), and endoscopic techniques (band ligation, sclerotherapy and clipping). Contributed by

Transabdominal color Doppler ultrasonography for the diagnosis of small intestinal and vesical varices in a patient successfully treated with percutaneous transhepatic obliteration.

A 52-year-old asymptomatic female was admitted to our hospital in January 2008 with enlarged esophageal varices due to alcoholic liver cirrhosis. Color Doppler ultrasonographic examination showed images of vessels on the small intestinal wall around the umbilical area and the anterior wall of the bladder. Images of the vessels were obtained for the small intestinal wall and the anterior wall of the bladder with computed tomography. Percutaneous transhepatic portography was performed, and hepatofugal blood flow was observed in the inferior epigastric vein connected to the superior mesenteric vein and the contrast medium passed into the small intestinal varices and the vesical varices, which drained into the right ovarian vein. Percutaneous transhepatic obliteration was then successfully performed via the afferent veins of the small intestinal varices and vesical varices. One week after the treatment, color Doppler ultrasonography showed a remarkable decrease in blood flow in the varices.

Color Doppler sonography and angioscintigraphy in hepatic Hodgkin’s lymphoma

To estimate the characteristics of Color Doppler findings and the results of hepatic radionuclide angiography (HRA) in secondary Hodgkin's hepatic lymphoma. The research included patients with a diagnosis of Hodgkin's lymphoma with metastatic focal lesions in the liver and controls. Morphologic characteristics of focal liver lesions and hemodynamic parameters were examined by pulsed and Color Doppler in the portal, hepatic and splenic veins were examined. Hepatic perfusion index (HPI) estimated by HRA was calculated. In the majority of patients, hepatomegaly was observed. Lesions were mostly hypoechoic and mixed, solitary or multiple. Some of the patients presented with dilated splenic veins and hepatofugal blood flow. A pulse wave was registered in the centre and at the margins of lymphoma. The average velocity of the pulse wave was higher at the margins (P > 0.05). A continuous venous wave was found only at the margins of lymphoma. There was no linear correlation between lymphoma size and velocity of pulse and continuous wave (r = 390, P < 0.01). HPI was significantly lower in patients with lymphomas than in controls (P < 0.05), pointing out increased arterial perfusion in comparison to portal perfusion. Color Doppler ultrasonography is a sensitive method for the detection of neovascularization in Hodgkin's hepatic lymphoma and estimation of its intensity. Hepatic radionuclide angiography can additionally help in the assessment of vascularisation of liver lesions.

Evaluation of non-target arterial patency after implantation of hepatic arterial catheter using a modified implantation technique with the fixed catheter tip method

To retrospectively investigate persistent hepatofugal blood flow in the gastroduodenal artery after implantation of a port-catheter system for repeated hepatic arterial infusion chemotherapy using a modified fixed catheter tip method. A port-catheter system was percutaneously implanted in 150 patients (90 men and 60 women; mean age 64.6 years) with unresectable liver cancer. The persistence of blood flow beyond the end hole of the indwelling catheter via the port obtained immediately and 1-10 days after port-catheter placement was investigated using arteriography. In all cases, port-catheter placement was successfully performed. In 64 (42.7%) of the 150 participants, the gastroduodenal artery was detected on arteriography just after implantation. However, arteriography obtained 1-10 days (mean 4.3 days) after implantation revealed the gastroduodenal artery in only two of the 64 participants. In these two patients, persistent blood flow disappeared spontaneously 12 and 15 days after implantation, respectively. Closure of the lumen of the distal tip of the catheter beyond the side hole most often occurs spontaneously just after implantation. However, the findings of the present study indicate that closure will occur within 15 days at the latest. This suggests that delaying chemotherapy for about 2 weeks after implantation may be advisable.

Efficacy of color Doppler ultrasonography for the diagnosis of duodenal varices successfully treated with percutaneous transhepatic obliteration

We treated a 74-year-old woman who complained of tarry stool. Neither endoscopic examination of the upper gastrointestinal tract nor colonoscopy revealed any finding indicative of bleeding, and (99m)Tc-HSA-D pool scintigraphic imaging showed no accumulation of blood in the digestive tract. Small tortuous collateral veins were observed on computed tomography (CT) in the distal third portion of the duodenum. Color Doppler ultrasonography obtained color flow images of varices in the distal third portion of the duodenum indicating turbulent flow, and color flow imaging showed the outflow vessel from duodenal varices. Duodenoscopy revealed tortuous varices, with erosions and blue in appearance, in the same area. Percutaneous transhepatic portography was carried out 18 days after the treatment of ascites, and hepatofugal blood flow was confirmed in the pancreatic duodenal vein originating near the junction between the splenic and inferior mesenteric veins with the passage of contrast medium into the duodenal varices, which drained into the left ovarian vein. We performed selective catheterization into the afferent vein of the varices, and injected 8 ml of a 5% solution of ethanolamine oleate containing iopamidol. Microcoil embolization using steel coils was added because the therapeutic effect resulting after the relatively rapid washout of sclerosant was insufficient. CT and color Doppler ultrasonography showed absence of blood flow in the varices 1 week after the therapy. This patient has had no episodes of rebleeding in the 24 months after therapy. Color Doppler ultrasonography was useful in diagnosing this case of duodenal varices and in evaluating therapeutic effect.

DIAGNOSIS OF ARTERIOPORTAL FISTULAE IN FOUR DOGS USING COMPUTED TOMOGRAPHIC ANGIOGRAPHY

Arterioportal fistulae are rare congenital anomalies of the hepatic vasculature. Diagnosis is conventionally made by selective angiography or ultrasonography. This report describes use of a dual-phase computed tomographic (CT) angiographic technique to diagnose arterioportal fistulae in four dogs. Advantages of this method include a noninvasive peripheral injection of contrast medium, ability to diagnose multiple acquired extrahepatic shunts, and observation of hemodynamic changes such as hepatofugal blood flow and reduced circulation to the caudal abdomen. The hepatic vasculature including arteries, veins, and portal veins can be completely evaluated. Dual-phase CT angiography is a safe and minimally invasive method of diagnosing arterioportal fistulae in dogs.

Management of End Hole in Placement of Port-Catheter System for Continuous Hepatic Arterial Infusion Chemotherapy Using the Fixed Catheter Tip Method

The purpose of our study was to compare persistent hepatofugal blood flow in the gastroduodenal artery after implanting a port-catheter system for repeated hepatic arterial infusion chemotherapy using either the original or the modified fixed catheter tip method. With the original method the lumen of the catheter tip is closed with a microcoil; with the modified method it is left open. Persistent hepatofugal blood flow can induce reactive gastric or duodenal mucosal lesions. A port-catheter system with the catheter tip fixed to the gastroduodenal artery by embolic agents was percutaneously implanted in 156 patients (102 men, 54 women; mean age, 63.2 years) with unresectable liver cancer. In 98 patients the original method was used, and in 58 patients the modified method was used. Existence of persistent blood flow beyond the indwelling catheter tip as shown on arteriography via the port performed immediately and 2-10 days after port-catheter placement was compared between these two groups. In all cases, percutaneous port-catheter placement was successfully performed. In one (1.0%) of 98 procedures involving the original method, the gastroduodenal artery was detected on arteriography just after implantation, compared with 23 (39.7%) of 58 procedures using the modified method. However, arteriography performed 2-10 days (mean, 5.02 days) after implantation detected the gastroduodenal artery in only one case. This retrospective study indicates that closure of the end hole appears to occur spontaneously shortly after implantation. Thus, such closure is not always necessary to avoid persistent hepatofugal blood flow in the gastroduodenal artery.

Hemodynamic analysis of esophageal varices in patients with liver cirrhosis using color Doppler ultrasound

To study the portal hemodynamics and their relationship with the size of esophageal varices seen at endoscopy and to evaluate whether these Doppler ultrasound parameters might predict variceal bleeding in patients with liver cirrhosis and portal hypertension. One hundred and twenty cirrhotic patients with esophageal varices but without any previous bleeding were enrolled in the prospective study. During a 2-year observation period, 52 patients who had at least one episode of acute esophageal variceal hemorrhage constituted the bleeding group, and the remaining 68 patients without any previous hemorrhage constituted the non-bleeding group. All patients underwent endoscopy before or after color Doppler-ultrasonic examination, and images were interpreted independently by two endoscopists. The control group consisted of 30 healthy subjects, matched to the patient group in age and gender. Measurements of diameter, flow direction and flow velocity in the left gastric vein (LGV) and the portal vein (PV) were done in all patients and controls using color Doppler unit. After baseline measurements, 30 min after oral administration of 75 g glucose in 225 mL, changes of the diameter, flow velocity and direction in the PV and LGV were examined in 60 patients with esophageal varices and 15 healthy controls. The PV and LGV were detected successfully in 115 (96%) and 105 (88%) of 120 cirrhotic patients, respectively, and in 27 (90%) and 21 (70%) of 30 healthy controls, respectively. Among the 120 cirrhotic patients, 37 had F1, 59 had F2, and 24 had F3 grade varices. Compared with the healthy controls, cirrhotic group had a significantly lower velocity in the PV, a significantly greater diameter of the PV and LGV, and a higher velocity in the LGV. In the cirrhotic group, no difference in portal flow velocity and diameter were observed between patients with or without esophageal variceal bleeding (EVB). However, the diameter and blood flow velocity of the LGV were significantly higher for EVB (+) group compared with EVB (-) group (P < 0.01). Diameter of the LGV increased with enlarged size of varices. There were differences between F1 and F2, F1 and F3 varices, but no differences between F2 and F3 varices (P = 0.125). However, variceal bleeding was more frequent in patients with a diameter of LGV >6 mm. The flow velocity in the LGV of healthy controls was 8.70+/-1.91 cm/s (n = 21). In patients with liver cirrhosis, it was 10.3+/-2.1 cm/s (n = 12) when the flow was hepatopetal and 13.5+/-2.3 cm/s (n = 87) when it was hepatofugal. As the size of varices enlarged, hepatofugal flow velocity increased (P < 0.01) and was significantly different between patients with F1 and F2 varices and between patients with F2 and F3 varices. Variceal bleeding was more frequent in patients with a hepatofugal flow velocity >15 cm/s (32 of 52 patients, 61.5%). Within the bleeding group, the mean LGV blood flow velocity was 16.6+/-2.62 cm/s. No correlation was observed between the portal blood flow velocity and EVB. In all healthy controls, the flow direction in the LGV was hepatopetal, toward the PV. In patients with F1 varices, flow direction was hepatopetal in 10 patients, to-and-fro state in 3 patients, and hepatofugal in the remaining 18. The flow was hepatofugal in 91% patients with F2 and all F3 varices. Changes in diameter of the PV and LGV were not significant before and after ingestion of glucose (PV: 1.41+/-1.5 cm before and 1.46+/-1.6 cm after; LGV: 0.57+/-1.7 cm before and 0.60+/-1.5 cm after). Flow direction in the LGV was hepatopetal and to-and-fro in 16 patients and hepatofugal in 44 patients before ingestion of glucose. Flow direction changed to hepatofugal in 9 of 16 patients with hepatopetal and to-and-fro blood flow after ingestion of glucose. In 44 patients with hepatofugal blood flow in the LGV, a significant increase in hepatofugal flow velocity was observed in 38 of 44 patients (86%) with esophageal varices. There was a relationship between the percentage changes in flow velocity and the size of varices. Patients who responded excessively to food ingestion might have a high risk for bleeding. The changes of blood flow velocity in the LGV were greater than those in the PV (LGV: 28.3+/-26.1%, PV: 7.2+/-13.2%, P < 0.01), whereas no significant changes in the LGV occurred before and after ingestion of glucose in the control subjects. Hemodynamics of the PV is unrelated to the degree of endoscopic abnormalities in patients with liver cirrhosis. The most important combinations are endoscopic findings followed by the LGV hemodynamics. Duplex-Doppler ultrasonography has no value in the identification of patients with cirrhosis at risk of variceal bleeding. Hemodynamics of the LGV appears to be superior to those of the PV in predicting bleeding.

Hemodynamic response of the left gastric vein to glucagon in patients with portal hypertension and esophageal varices

Flow direction and flow velocity of the left gastric vein (LGV) and the portal vein (PV) were examined by a Doppler sonographic machine in 33 patients with esophageal varices, before and after venous injection of glucagon (1 mg). In two patients with hepatopetal blood flow in the LGV, the flow direction changed to hepatofugal after injection of glucagon. In 31 patients with hepatofugal blood flow in the LGV, a significant increase of flow velocity was observed in the LGV in 18 patients (58.1%) and the changes (26.4 ± 24.6%) were significantly larger than those in the PV (7.9 ± 16.0%). The changes in flow velocity decreased in the LGV as the diameter of the LGV and the size of varices increased. In conclusion, glucagon increased collateral blood flow in the LGV in portal hypertension. However, the grade of the response decreased as the grade of portal hypertension increased. (E-mail: matsu@med.m.chiba-u.ac.jp)

Hemodynamic assessment of the left gastric vein in patients with esophageal varices with color Doppler EUS: Factors affecting development of esophageal varices

Background: An understanding of the development of esophageal varices is important in the evaluation of risk of variceal hemorrhage. To clarify factors affecting the development of esophageal varices, the morphology and hemodynamics of the left gastric vein were analyzed with color Doppler EUS. Methods: Sixty-seven patients with esophageal varices underwent color Doppler EUS. Seventeen had small varices (F1), 32 had medium varices (F2), and 18 had large varices (F3). Results: Hepatofugal blood flow velocity in the left gastric vein trunk increased as the size of the varices increased (p < 0.0001), whereas the diameter did not increase. The left gastric vein bifurcates into anterior and posterior branches. As the size of the varices enlarged, the branch pattern was more likely to be anterior branch dominant (p = 0.041). There was no significant difference between the 3 size groups of esophageal varices with respect to the size of the paraesophageal collaterals. The detection rate and diameter of the perforating vein increased as the size of the varices increased (p = 0.032 and 0.012, respectively). Conclusion: Blood flow velocity in the left gastric vein trunk, branches, and perforating veins may regulate blood flow supplying the esophageal varices and contribute to their development. These findings are important to understanding the pathogenesis of esophageal varices. (Gastrointest Endosc 2002;55:512-7.)

Response of blood flow to vasopressin in the collateral left gastric vein in patients with portal hypertension

Background/Aims: A problem in pharmacotherapy for bleeding varices in portal hypertension is non-responders. The aim of this study was to elucidate the features of hemodynamic response to vasopressin in the gastroesophageal collateral vein in patients with esophageal varices. Methods: Flow velocity in the portal and the collateral left gastric vein was measured with an echo-Doppler flowmeter before and during infusion of vasopressin, 0.2 U/min, in 41 patients with cirrhois and esophageal varices. Results: The decrease in flow velocity in the left gastric vein with vasopressin (–29±25%) was significantly smaller than that in the portal vein (–56±20%). There was no or only minimal change in flow velocity in the left gastric vein in 39% of the patients, especially in those with large-size varices. In 28 patients examined by portal catheterization, changes in flow velocity in the left gastric vein were correlated with portal pressure, and portal pressure in non-responders was significantly higher than that in responders (non-responders: 363±49, responders: 312±41 mmH 2O, p<0.05). Conclusions: It was concluded that hepatofugal blood flow in the gastroesophageal collateral is not readily reduced by vasopression. However, as the study was performed in a stable condition without variceal bleeding, whether these hemodynamic features will apply during acute variceal bleeding in patients who are known to have a poor hemodynamic response to vasopressin remains to be elucidated.

Influence of spontaneous portosystemic collateral pathways on portal hemodynamics in living-related liver transplantation in children. Doppler ultrasonographic study.

We investigated the influence of spontaneous portosystemic collateral pathways on the portal hemodynamics and examined the necessity for ligating these vessels in pediatric liver transplantation from living donors. We assessed portal blood flow before, during, and after surgery in 82 pediatric recipients (mean age, 4.2 years), using Doppler ultrasonography. When blood flow in the reconstructed portal vein was decreased (< 10 ml/min/kg body weight) and portosystemic collaterals persisted during surgery, those vessels were ligated and Doppler flowmetry was examined again. Spontaneous portosystemic collaterals were detected at one or more sites in 67 patients before transplantation. These collaterals had been ligated in 17 patients before intraoperative flowmetry. Among the remaining 50 patients, initial Doppler studies revealed a decrease in portal blood flow in 22 patients. Nine patients had hepatofugal splenic venous flow and 6 had no significant flow signals from the intrahepatic portal vein. Ligation of collaterals resulted in a remarkable increase in portal blood flow in 20 patients, all of whom are alive. The remaining 2 patients died of graft failure due in part to portal hypoperfusion. On the other hand, the collaterals were not ligated in 24 patients because adequate portal blood flow was confirmed by intraoperative flowmetry. Postoperatively, flow signals from the unligated collateral vessels gradually diminished, but they still persisted in 3 patients at 12 months after transplantation. Hepatofugal blood flow through the portosystemic collateral pathways may persist after implantation of a normal graft. If the patent collaterals significantly reduce the effective portal blood flow, these vessels should be ligated in order to avoid graft failure.

Hemodynamics of the left gastric vein in portal hypertension

Background: Esophageal varices reflect the hemodynamics of the left gastric vein, which can now be studied by Doppler ultrasonography. The purpose of this study was to elucidate the hemodynamic features of the left gastric vein in portal hypertension. Methods: Flow direction and velocity in the left gastric vein were examined by the pulsed Doppler flowmeter in 53 healthy adults and 216 patients with liver cirrhosis. Results: Flow direction was hepatopetal in all healthy controls, whereas it was hepatofugal in 72% of the patients with esophageal varices. In the early stage of mild esophageal varices, flow direction was still hepatopetal. However, in portal pressure > 250 mm H2O, hepatofugal flow was highly frequent (56 of 59 patients, 95%). Hepatofugal flow velocity in patients with varices was 8.5 ± 2.5 cm/s in mild varices, 11.6 ± 2.4 cm/s in intermediate varices, and 13.8 ± 3.4 cm/s in marked varices. Variceal bleeding was frequent in patients with a flow velocity > 15 cm/s (7 of 14 patients, 50%). Flow velocity in the left gastric vein increased after ingestion of glucose in 43 of 56 patients with esophageal varices. Conclusions: In portal hypertension, as the size of varices enlarged, hepatofugal blood flow in the left gastric vein increased in parallel. High flow velocity in the left gastric vein was strongly associated with variceal bleeding. Increase of blood flow after ingestion of glucose suggests postprandial increase in variceal flow.

Total hepatofugal portal blood flow in cirrhosis demonstrated by transhepatic portography.

We investigated 108 patients with cirrhosis of the liver and portal hypertension by percutaneous transhepatic portography to demonstrate the occurrence and frequency of total hepatofugal portal blood flow. Sixteen patients (14.8%) had a total hepatofugal portal blood flow. The aetiology of portal hypertension and the portal pressure did not differ from that in the group of patients with hepatopetal portal blood flow. A significantly higher percentage of patients in the group with hepatofugal flow had gastro-oesophageal varices (P less than 0.025). All patients with varices had bled. Half of the patients in the group with hepatofugal blood flow had a false splenoportographic diagnosis of portal vein thrombosis. In conclusion, total hepatofugal postal blood flow exists more often than hitherto assumed. Hepatofugal blood flow does not relieve portal hypertension nor prevent development of gastrooesophageal varices or bleeding.