Abstract
analyzed. In 6 patients ESLD was due to biliary atresia, mean age 44 months (range 8−60), the remaining 5 to miscellaneous causes (one patient to Wilson’s disease, one biliary cirrhosis, one congenital hepatic fibrosis, one cryptogenic chronic hepatitis, one acute liver failure of unknown origin), mean age 127 months (range 72–191). 9 out of 11 patients had varices. 6 patients had F1 esophageal varices, 1 patient had F3 esophageal varices, two patients with no esophageal varices on EGDS had large perigastric and peri-esophageal varices detected on CT scan. Results: Catheterization of hepatic veins was done under deep sedation and was technically possible in all patients without complications. HVPG values were elevated in all patients, ranging between 8 and 33mmHg (mean 13.5mmHg), thus indicating a sinusoidal component in the portal hypertension. A salient finding was the presence of hepatic venous-venous shunts in 5 out of 6 patients with biliary atresia; these were identical to those described in idiopathic portal hypertension. The presence of venousvenous shunts frequently precludes adequate HVPG measurements; however HVPG could still be measured distally to the shunts in 4 patients using ultrathin catheters, but in two patients (both HVPG 8mmHg) was determined in an area with a small venous-venous communication still visible, therefore underestimating the actual portal pressure gradient. Actually both patients had esophageal varices. No venous-venous shunts were detected in the non biliary atresia patients. Conclusion: HVPG is a feasible procedure in pediatric patients. Patients with biliary atresia very frequently have venous-venous shunts between hepatic veins. This hitherto unrecognized finding can lead to underestimation of the portal pressure by HVPG measurement.
Published Version
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