ORIGINAL ARTICLE
Influence of Paraumbilical Vein Patency on the Portal Hemodynamics of Patients With Cirrhosis Takayuki Kondo, MD,* Hitoshi Maruyama, MD, PhD,* Tadashi Sekimoto, MD,* Taro Shimada, MD, PhD,* Masanori Takahashi, MD, PhD,* Hidehiro Okugawa, MD, PhD,* Osamu Yokosuka, MD, PhD,* and Tadashi Yamaguchi, Dr Engw
Goals/Background: The aim was to determine the influence of the paraumbilical vein (PUV) patency and its effect on the portal hemodynamics and clinical presentations in cirrhotic patients. Study: In this prospective study of 181 cirrhotic patients (101 males, 80 females; aged 62.6 ± 11.8 y), the portal hemodynamics were assessed using Doppler ultrasonography. Results: The incidence of patent PUV was 26.0% (47/181). The mean flow volume in the portal trunk, the incidence of a left gastric vein with hepatofugal flow, and the grade of the esophageal varices were significantly higher in the patients with a patent PUV (908.2 mL/min, 70.2%, 9 with none to small, and 27 with medium to large, respectively) than in those without (771.7 mL/min, 48.5%, 57 with none to small, and 48 with medium to large, respectively). The hepatic venous pressure gradient and the wedged hepatic venous pressure (mm H2O) were significantly higher in the former group (268.0 ± 89.7 and 389.5 ± 99.9, respectively) than in the latter (203.5 ± 63.2 and 317.7 ± 67.7, respectively). The deterioration of ascites during the 2-year follow-up period was significantly more often in the patients with a patent PUV (4/12, 33.3%) than in those without. The cumulative survival rates at 1, 2, and 3 years were similar between the 2 groups: 92.5%, 92.5%, and 82.4%, respectively, in the former and 90.7%, 83.8%, and 76.3%, respectively, in the latter. Conclusions: A patent PUV seems to signify pressure-loaded portal hemodynamics in cirrhotic patients. However, it seems to have little effect on their prognoses. Key Words: cirrhosis, Doppler ultrasound, portal hypertension, paraumbilical vein
circulation, which is characterized by the systemic and splanchnic vasodilatation, low systemic resistance, plasma volume expansion, and a high cardiac index.3 Developing portal-collateral circulation is one of the hemodynamic features of portal hypertension. Forming collaterals is a complex process that involves the opening, dilatation, and hypertrophy of preexisting vascular channels.4,5 Collaterals develop in response to increased pressure, and a minimum threshold level of the hepatic venous pressure gradient (HVPG) of 10 mm Hg is needed to induce the development of portosystemic collaterals and esophageal varices.6 The paraumbilical vein (PUV) is a vessel in the falciform ligament, which is involved in fetal circulation. The incidence of a patent PUV is reportedly 11.1% in adult cirrhotic patients.7 Collateral vessels act to reduce the substantial portal flow in the liver. However, because the PUV tends to increase blood flow to the portal trunk,8 the portal hemodynamics caused by developing the patent PUV differ from those affected by other collateral vessels. Because of this unique anatomic feature, a patent PUV can result in an underestimation of the degree of portal hypertension.8 However, the role and effects of a patent PUV with respect to the portal hemodynamics remain unclear. This study was designed to determine how a patent PUV influences the portal venous pressure and how it changes the longitudinal clinical course of cirrhosis. The study’s aim was to elucidate the influence of the PUV patency and its effect on the portal hemodynamics and clinical presentations of cirrhotic patients.
(J Clin Gastroenterol 2014;48:178–183)
MATERIALS AND METHODS
P
ortal hypertension is directly related to the outflow resistance and an increased portal inflow.1 In cirrhosis, the outflow resistance depends on the severity of the liver damage, mechanical obstruction caused by the fibrotic disruption of the liver architecture, and a dynamic component produced by the active contraction of vascular smooth muscle cells and activated stellate cells.2 Meanwhile, the portal inflow is affected by the hyperdynamic Received for publication December 27, 2012; accepted July 7, 2013. From the *Department of Gastroenterology and Hepatology, Chiba University Graduate School of Medicine, Inohana, Chuou-ku; and wDepartment of Research Center for Frontier Medical Engineering, Chiba University, Yayoicho, Inage-ku, Chiba, Japan. The authors declare that they have nothing to disclose. Reprints: Hitoshi Maruyama, MD, PhD, Department of Gastroenterology and Hepatology, Chiba University Graduate School of Medicine, 1-8-1, Inohana, Chuou-ku, Chiba 260-8670, Japan (e-mail: [email protected]). Copyright r 2013 by Lippincott Williams & Wilkins
178 | www.jcge.com
Patients This prospective study was performed at Chiba University Hospital after approval by the ethics committee. Written informed consent was obtained from all of the patients. The study included consecutive cirrhotic patients with portal hypertension who received a Doppler ultrasound (US) examination to evaluate their portal hemodynamics from April 2007 to June 2012. The diagnosis of cirrhosis was based on a combination of biochemical findings and the US examination. The following exclusion criteria were applied: (1) patients with malignant hepatic lesions; (2) patients with vascular abnormalities, such as an intrahepatic arterioportal shunt diagnosed by a Doppler US examination; (3) patients with cavernomas diagnosed by an US examination; (4) patients using vasoactive drugs, such as b-blockers, because using such drugs for portal hypertension is not approved in our country (the patients who took these drugs for other reasons were also excluded from the study because the medication might affect their portal J Clin Gastroenterol
Volume 48, Number 2, February 2014
J Clin Gastroenterol
Volume 48, Number 2, February 2014
hemodynamics); (5) patients receiving antiviral therapy during the study period; and (6) patients who underwent interventional procedures, such as a transjugular intrahepatic portosystemic shunt or a peritoneovenous shunt. Gastroesophageal varices were classified according to the general rules of the Japan Research Society for Portal Hypertension9: straight (F1, small), winding (F2, medium), and nodule beaded (F3, large). The variceal appearance was assessed according to the endoscopic findings taken within 6 months before/after the Doppler study in the patients without treatment histories for varices. Hepatic encephalopathy was assessed using the West-Haven grading system,10 and a West-Haven grade II or above was classified as overt hepatic encephalopathy. The degree of ascites was defined according to the international guidelines11: mild for ascites that were only detectable by US examination, moderate for ascites that caused moderate symmetrical distention of the abdomen, and severe for ascites that caused marked abdominal distension. Changes in the degree of ascites were observed using US examinations at least once per year and by physical examinations at least twice per year. The patients with ascites were treated according to the guidelines,11 using diuretics under a saltrestricted diet with occasional paracentesis; the patients who underwent interventional radiology, such as a peritoneovenous shunt or a transjugular intrahepatic portosystemic shunt, were not included in our study. The observation period was defined as the time between the initial US examination and the date of the last hospital visit, death, or liver transplantation.
US Examination The US equipment was a SSA-770 A or a SSA-790 A (Toshiba) with a 3.75 MHz convex probe. The examination was performed with the patients placed in the supine position after fasting for >4 hours, and the patients were asked to breathe gently during the procedure. The portal hemodynamics were evaluated using both pulsed and color Doppler US.12 The diameter (mm), flow direction, mean flow velocity (cm/s), and flow volume (mL/ min) were measured at the portal trunk, splenic vein, superior mesenteric vein, and collateral vessels (Fig. 1). The blood flow measurement was taken at a
Influence of Paraumbilical Vein Patency on the Portal Hemodynamics of Patients With Cirrhosis Takayuki Kondo, MD,* Hitoshi Maruyama, MD, PhD,* Tadashi Sekimoto, MD,* Taro Shimada, MD, PhD,* Masanori Takahashi, MD, PhD,* Hidehiro Okugawa, MD, PhD,* Osamu Yokosuka, MD, PhD,* and Tadashi Yamaguchi, Dr Engw
Goals/Background: The aim was to determine the influence of the paraumbilical vein (PUV) patency and its effect on the portal hemodynamics and clinical presentations in cirrhotic patients. Study: In this prospective study of 181 cirrhotic patients (101 males, 80 females; aged 62.6 ± 11.8 y), the portal hemodynamics were assessed using Doppler ultrasonography. Results: The incidence of patent PUV was 26.0% (47/181). The mean flow volume in the portal trunk, the incidence of a left gastric vein with hepatofugal flow, and the grade of the esophageal varices were significantly higher in the patients with a patent PUV (908.2 mL/min, 70.2%, 9 with none to small, and 27 with medium to large, respectively) than in those without (771.7 mL/min, 48.5%, 57 with none to small, and 48 with medium to large, respectively). The hepatic venous pressure gradient and the wedged hepatic venous pressure (mm H2O) were significantly higher in the former group (268.0 ± 89.7 and 389.5 ± 99.9, respectively) than in the latter (203.5 ± 63.2 and 317.7 ± 67.7, respectively). The deterioration of ascites during the 2-year follow-up period was significantly more often in the patients with a patent PUV (4/12, 33.3%) than in those without. The cumulative survival rates at 1, 2, and 3 years were similar between the 2 groups: 92.5%, 92.5%, and 82.4%, respectively, in the former and 90.7%, 83.8%, and 76.3%, respectively, in the latter. Conclusions: A patent PUV seems to signify pressure-loaded portal hemodynamics in cirrhotic patients. However, it seems to have little effect on their prognoses. Key Words: cirrhosis, Doppler ultrasound, portal hypertension, paraumbilical vein
circulation, which is characterized by the systemic and splanchnic vasodilatation, low systemic resistance, plasma volume expansion, and a high cardiac index.3 Developing portal-collateral circulation is one of the hemodynamic features of portal hypertension. Forming collaterals is a complex process that involves the opening, dilatation, and hypertrophy of preexisting vascular channels.4,5 Collaterals develop in response to increased pressure, and a minimum threshold level of the hepatic venous pressure gradient (HVPG) of 10 mm Hg is needed to induce the development of portosystemic collaterals and esophageal varices.6 The paraumbilical vein (PUV) is a vessel in the falciform ligament, which is involved in fetal circulation. The incidence of a patent PUV is reportedly 11.1% in adult cirrhotic patients.7 Collateral vessels act to reduce the substantial portal flow in the liver. However, because the PUV tends to increase blood flow to the portal trunk,8 the portal hemodynamics caused by developing the patent PUV differ from those affected by other collateral vessels. Because of this unique anatomic feature, a patent PUV can result in an underestimation of the degree of portal hypertension.8 However, the role and effects of a patent PUV with respect to the portal hemodynamics remain unclear. This study was designed to determine how a patent PUV influences the portal venous pressure and how it changes the longitudinal clinical course of cirrhosis. The study’s aim was to elucidate the influence of the PUV patency and its effect on the portal hemodynamics and clinical presentations of cirrhotic patients.
(J Clin Gastroenterol 2014;48:178–183)
MATERIALS AND METHODS
P
ortal hypertension is directly related to the outflow resistance and an increased portal inflow.1 In cirrhosis, the outflow resistance depends on the severity of the liver damage, mechanical obstruction caused by the fibrotic disruption of the liver architecture, and a dynamic component produced by the active contraction of vascular smooth muscle cells and activated stellate cells.2 Meanwhile, the portal inflow is affected by the hyperdynamic Received for publication December 27, 2012; accepted July 7, 2013. From the *Department of Gastroenterology and Hepatology, Chiba University Graduate School of Medicine, Inohana, Chuou-ku; and wDepartment of Research Center for Frontier Medical Engineering, Chiba University, Yayoicho, Inage-ku, Chiba, Japan. The authors declare that they have nothing to disclose. Reprints: Hitoshi Maruyama, MD, PhD, Department of Gastroenterology and Hepatology, Chiba University Graduate School of Medicine, 1-8-1, Inohana, Chuou-ku, Chiba 260-8670, Japan (e-mail: [email protected]). Copyright r 2013 by Lippincott Williams & Wilkins
178 | www.jcge.com
Patients This prospective study was performed at Chiba University Hospital after approval by the ethics committee. Written informed consent was obtained from all of the patients. The study included consecutive cirrhotic patients with portal hypertension who received a Doppler ultrasound (US) examination to evaluate their portal hemodynamics from April 2007 to June 2012. The diagnosis of cirrhosis was based on a combination of biochemical findings and the US examination. The following exclusion criteria were applied: (1) patients with malignant hepatic lesions; (2) patients with vascular abnormalities, such as an intrahepatic arterioportal shunt diagnosed by a Doppler US examination; (3) patients with cavernomas diagnosed by an US examination; (4) patients using vasoactive drugs, such as b-blockers, because using such drugs for portal hypertension is not approved in our country (the patients who took these drugs for other reasons were also excluded from the study because the medication might affect their portal J Clin Gastroenterol
Volume 48, Number 2, February 2014
J Clin Gastroenterol
Volume 48, Number 2, February 2014
hemodynamics); (5) patients receiving antiviral therapy during the study period; and (6) patients who underwent interventional procedures, such as a transjugular intrahepatic portosystemic shunt or a peritoneovenous shunt. Gastroesophageal varices were classified according to the general rules of the Japan Research Society for Portal Hypertension9: straight (F1, small), winding (F2, medium), and nodule beaded (F3, large). The variceal appearance was assessed according to the endoscopic findings taken within 6 months before/after the Doppler study in the patients without treatment histories for varices. Hepatic encephalopathy was assessed using the West-Haven grading system,10 and a West-Haven grade II or above was classified as overt hepatic encephalopathy. The degree of ascites was defined according to the international guidelines11: mild for ascites that were only detectable by US examination, moderate for ascites that caused moderate symmetrical distention of the abdomen, and severe for ascites that caused marked abdominal distension. Changes in the degree of ascites were observed using US examinations at least once per year and by physical examinations at least twice per year. The patients with ascites were treated according to the guidelines,11 using diuretics under a saltrestricted diet with occasional paracentesis; the patients who underwent interventional radiology, such as a peritoneovenous shunt or a transjugular intrahepatic portosystemic shunt, were not included in our study. The observation period was defined as the time between the initial US examination and the date of the last hospital visit, death, or liver transplantation.
US Examination The US equipment was a SSA-770 A or a SSA-790 A (Toshiba) with a 3.75 MHz convex probe. The examination was performed with the patients placed in the supine position after fasting for >4 hours, and the patients were asked to breathe gently during the procedure. The portal hemodynamics were evaluated using both pulsed and color Doppler US.12 The diameter (mm), flow direction, mean flow velocity (cm/s), and flow volume (mL/ min) were measured at the portal trunk, splenic vein, superior mesenteric vein, and collateral vessels (Fig. 1). The blood flow measurement was taken at a
