Home About us Contact | |||
Portal Venous Flow (portal + venous_flow)
Selected AbstractsRisk factors for portal venous thrombosis after splenectomy in patients with cirrhosis and portal hypertensionBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 6 2010N. Kinjo Background: Portal venous thrombosis (PVT) is a potentially fatal complication following splenectomy. Its mechanisms and risk factors are poorly understood, especially in patients with cirrhosis and portal hypertension. This study investigated risk factors for PVT following splenectomy in such patients. Methods: All consecutive patients with cirrhosis who underwent splenectomy in Kyushu University Hospital between 1998 and 2004 were included in this retrospective study. They were divided into two groups based on the presence or absence of postoperative PVT. Preoperative and operative factors were compared, and the relationships between formation of PVT and its independent variables were analysed. In some cases, portal venous flow was measured before and after splenectomy using duplex Doppler ultrasonography. Results: PVT developed after surgery in 17 (24 per cent) of 70 patients studied. Multivariable analysis showed that increased splenic vein diameter and low white cell count were significant independent risk factors for PVT. Portal venous flow after splenectomy was greatly reduced in the PVT group, but not in patients without PVT. Conclusion: Large splenic vein diameter and low white cell count are independent risk factors for PVT after splenectomy in patients with cirrhosis and portal hypertension. Copyright © 2010 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] Scintigraphic evaluation of intrapulmonary shunt in normoxemic cirrhotic patients and effects of terlipressinHEPATOLOGY RESEARCH, Issue 10 2010George Kalambokis Aim:, The magnitude of intrapulmonary shunt (IPS) in cirrhotic patients without hypoxemia remains undefined. We evaluated the severity and clinical correlations of IPS in normoxemic cirrhotics, and possible IPS alterations after terlipressin treatment. Methods:, Fifteen patients with alcoholic cirrhosis without hypoxemia were studied at baseline and after the administration of 2 mg of terlipressin. The IPS fraction was evaluated by lung perfusion scan after the i.v. injection of technetium-99m -labeled macroaggregated albumin (99mTc-MAA) and calculation of brain uptake (positive value ,6%). Cardiac output (CO), pulmonary artery systolic pressure (PASP) and pulmonary vascular resistance (PVR) were evaluated by Doppler echocardiography. Mean arterial pressure (MAP) was measured and the ratio MAP/CO was calculated as an index of systemic vascular resistance (SVR). Portal vein velocity (PVV) and portal venous flow (PVF) were also assessed by Doppler ultrasonography. Results:, Three patients (20%) had an IPS fraction of more than 6%. A significant inverse correlation with platelet count (P = 0.001) and a direct correlation with Child,Pugh score (P = 0.06), PVV (P = 0.07) and PVF (P = 0.07) were noted. IPS fractions decreased significantly after terlipressin administration (P = 0.00001); the IPS fraction fell below 6% in all three patients with positive baseline values. Terlipressin treatment induced a significant decrease in CO (P = 0.003) and significant increases in MAP (P = 0.0003), SVR (P = 0.0003), SPAP (P = 0.001) and PVR (P = 0.01). Conclusion:, IPS fractions detected by 99mTc-MAA lung scan were inversely correlated with platelet count and directly with liver disease severity, and found abnormal in 20% of normoxemic cirrhotic patients. Terlipressin reduced significantly the magnitude of the shunt. [source] Color Doppler sonographic signs of respiration-dependent hepatofugal portal flowJOURNAL OF CLINICAL ULTRASOUND, Issue 2 2004Christian Görg MD Abstract Purpose The role of respiration in modulating blood flow in the portal vein is unclear. The aim of this study was to investigate the phenomenon of respiration-dependent periodic hepatofugal portal venous blood flow as detected on color Doppler sonography. Methods Within 1 year, we identified 13 patients with respiration-dependent reversal of blood flow in the portal vein that was diagnosed on color Doppler sonography. This phenomenon was investigated by color Doppler sonographic examination of the portal venous flow during both mid-inspiration breath-holding and a respiratory cycle including deep inspiration; evaluation of hepatic vein Doppler waveforms as normal (triphasic) or decreased (flattened); and echocardiographic examination to determine the presence or absence of tricuspid regurgitation. Results The patients' median age was 53 years (range, 26,87 years). Seven of the 13 patients had heart disease (tricuspid regurgitation) with or without liver disease, 3 had liver disease without heart disease, and 3 had other diseases with no evidence of heart or liver disease. On Doppler sonography, 10 of the 13 patients had increased portal venous pulsatility (7 of the 10 had tricuspid regurgitation; the other 3 did not); the remaining 3 patients had neither increased pulsatility nor tricuspid regurgitation. Sonographic follow-up within 4 weeks in 4 of the 13 patients revealed loss of the respiration-dependent hepatofugal portal flow. Conclusions Respiration-dependent hepatofugal portal flow is a rare finding associated with periodic portal hypertension in patients with right heart insufficiency and liver disease. Its clinical significance is unclear. Among our patients, its occurrence was predominantly associated with an increased venous pulsatility index due to tricuspid regurgitation or venous outflow obstruction. Further study is needed to investigate whether periodic respiration-dependent hepatofugal portal flow is predictive of the occurrence of continuous flow reversal. © 2004 Wiley Periodicals, Inc. J Clin Ultrasound 32:62,68, 2004 [source] Venous hemodynamics in living donor right lobe liver transplantationLIVER TRANSPLANTATION, Issue 9 2002Gabriel E. Gondolesi MD We evaluated the influence of portal and hepatic venous hemodynamics on the immediate and 3-month postoperative function of living donor right lobe grafts. Portal velocity was measured prospectively by ultrasound in 14 consecutive donor/recipient pairs. Velocity was converted to flow with the Moriyasu formula. Measurements were taken in donors in the operating room and in recipients at 1 hour after reperfusion and 3 months after transplant. Recipient liver function tests were measured postoperatively. Prereperfusion and postreperfusion liver biopsies were evaluated and correlated with the hemodynamic and biochemical results. There were 11 male (78.6%) and 3 female donors (mean age, 38.9 ± 9.8 years) for 10 male (71.4%) and 4 female recipients (mean age, 49.3 ± 14 years). The mean graft/recipient weight ratio was 1.22 ± 0.3. The mean right portal vein pressure was 8 ± 1.8 mm Hg in donors versus 13 ± 4.7 mm Hg in recipients (P < .05). The mean peak flow velocity (Vmax) in the portal vein in donors was 47.6 ± 12.8 cm/sec (normal, 44 cm/sec). One hour after graft reperfusion in the recipient, the mean portal Vmax was significantly higher at 94.7 ± 28.4 cm/sec (P = .004), but by 3 months follow-up, mean portal Vmax had fallen to 58.8 ± 37.8 (P = .01). Recipient portal vein Vmax highly correlated with portal flow (r = 0.7, P = .01). Increased recipient total bilirubin on postoperative day 2 correlated highly with higher recipient portal flow one hour after transplant (r = 0.6; P = .03). Portal vein velocity/flow dramatically increases after reperfusion, returning to baseline about 3 months after transplant. Evaluation of hepatic and portal venous flow is a relatively easy skill to acquire. Intraoperative ultrasound may enable the surgeon to predict graft dysfunction and possibly, may be used to implement pre-emptive therapies. [source] Liver Graft-to-Recipient Spleen Size Ratio as a Novel Predictor of Portal Hyperperfusion Syndrome in Living Donor Liver TransplantationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 12 2006Y.-F. Cheng Portal hyperperfusion in a small-size liver graft is one cause of posttransplant graft dysfunction. We retrospectively analyzed the potential risk factors predicting the development of portal hyperperfusion in 43 adult living donor liver transplantation recipients. The following were evaluated: age, body weight, native liver disease, spleen size, graft size, graft-to-recipient weight ratio (GRWR), total portal flow, recipient portal venous flow per 100 g graft weight (RPVF), graft-to-recipient spleen size ratio (GRSSR) and portosystemic shunting. Spleen size was directly proportional to the total portal flow (p = 0.001) and RPVF (p = 0.014). Graft hyperperfusion (RPVF flow >250 mL/min/100 g graft) was seen in eight recipients. If the GRSSR was <0.6, 5 of 11 cases were found to have graft hyperperfusion (p = 0.017). The presence of portosystemic shunting was significant in decreasing excessive RPVF (p = 0.059). A decrease in portal flow in the hyperperfused grafts was achieved by intraoperative splenic artery ligation or splenectomy. Spleen size is a major factor contributing to portal flow after transplant. The GRSSR is associated with posttransplant graft hyperperfusion at a ratio of <0.6. [source] Risk factors for portal venous thrombosis after splenectomy in patients with cirrhosis and portal hypertensionBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 6 2010N. Kinjo Background: Portal venous thrombosis (PVT) is a potentially fatal complication following splenectomy. Its mechanisms and risk factors are poorly understood, especially in patients with cirrhosis and portal hypertension. This study investigated risk factors for PVT following splenectomy in such patients. Methods: All consecutive patients with cirrhosis who underwent splenectomy in Kyushu University Hospital between 1998 and 2004 were included in this retrospective study. They were divided into two groups based on the presence or absence of postoperative PVT. Preoperative and operative factors were compared, and the relationships between formation of PVT and its independent variables were analysed. In some cases, portal venous flow was measured before and after splenectomy using duplex Doppler ultrasonography. Results: PVT developed after surgery in 17 (24 per cent) of 70 patients studied. Multivariable analysis showed that increased splenic vein diameter and low white cell count were significant independent risk factors for PVT. Portal venous flow after splenectomy was greatly reduced in the PVT group, but not in patients without PVT. Conclusion: Large splenic vein diameter and low white cell count are independent risk factors for PVT after splenectomy in patients with cirrhosis and portal hypertension. Copyright © 2010 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] |