Postprandial Portal Vein Flow in Portal Hypertension and after Distal Splenorenal Shunt
Donald L. Jacobs, Joseph C. Anderson, Robert A. Cormier, Layton F. Rikkers
Abstract
Donald L. Jacobs, Joseph C. Anderson, Robert A. Cormier, Layton F. Rikkers
Abstract
Postprandial portal vein flow (PVF) was measured using duplex ultrasound in healthy controls, patients with nonshunted portal hypertension and patients with distal splenorenal shunts (DSRS). In the fasting state, PVF was significantly greater in patients with portal hypertension (1,077 ± 45 ml/min) than in controls (672 ± 16 ml/min, p < 0.005) or in patients with DSRS (280 ± 30 ml/min, p < 0.005) and significantly greater in controls than in the DSRS group. After eating, only the controls showed significant increases in PVF (128 ± 8, 103 ± 9, and 47 ± 3% increase above fasting PVF at 30, 90, and 150 min, respectively; all p < 0.005). In portal hypertensive patients, eating did not result in a consistent change in PVF. In the fasting state, 6 DSRS patients had prograde flow and 4 had retrograde flow. Shunt patients with prograde flow had a response in PVF after eating similar to that seen in nonshunted portal hypertension patients (4 with increased and 2 with unchanged flow). None of the shunt patients with retrograde flow developed prograde flow after eating. In conclusion: (1) fasting PVF is greater in portal hypertension patients and less in DSRS patients compared to controls; (2) eating results in increased PVF in controls but no consistent response is seen in portal hypertension or in DSRS patients, and (3) DSRS patients with retrograde PVF do not convert to prograde flow after eating.
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Postprandial portal vein flow (PVF) was measured using duplex ultrasound in healthy controls, patients with nonshunted portal hypertension and patients with distal splenorenal shunts (DSRS). In the fasting state, PVF was significantly greater in patients with portal hypertension (1,077 ± 45 ml/min) than in controls (672 ± 16 ml/min, p < 0.005) or in patients with DSRS (280 ± 30 ml/min, p < 0.005) and significantly greater in controls than in the DSRS group. After eating, only the controls showed significant increases in PVF (128 ± 8, 103 ± 9, and 47 ± 3% increase above fasting PVF at 30, 90, and 150 min, respectively; all p < 0.005). In portal hypertensive patients, eating did not result in a consistent change in PVF. In the fasting state, 6 DSRS patients had prograde flow and 4 had retrograde flow. Shunt patients with prograde flow had a response in PVF after eating similar to that seen in nonshunted portal hypertension patients (4 with increased and 2 with unchanged flow). None of the shunt patients with retrograde flow developed prograde flow after eating. In conclusion: (1) fasting PVF is greater in portal hypertension patients and less in DSRS patients compared to controls; (2) eating results in increased PVF in controls but no consistent response is seen in portal hypertension or in DSRS patients, and (3) DSRS patients with retrograde PVF do not convert to prograde flow after eating.
Key concepts: Medicine, Postprandial, Portal hypertension, Internal medicine, Gastroenterology, Shunt (medical), Superior mesenteric vein, Portal vein