Patent ductus venosus: diagnosis by MR angiography

Abstract

We report a 15-year-old boy with patent ductus venosus in whom the diagnosis was made by MR angiography. A patent ductus venosus Arantii is a rare form of portosystemic shunt. Only a few cases have been reported in adults and children. The diagnosis is usually made by US and digital subtraction angiography. In our patient, the diagnosis was first made by MR angiography. This demonstrates the excellent diagnostic potential of the method in paediatric patients.

Congenital Portosystemic Shunts in Children: Recognition, Evaluation, and Management

“…Two studies use the results of neonatal screening for galactosemia after a few days of feeding to estimate the prevalence of congenital portosystemic shunts 144,145 : High concentrations of blood galactose, unexplained by an abnormal activity of the enzymes of galactose metabolism, can be found in neonates 11,16,24,25,27,29,38,41,44,51,53,55,59,64,68,70,76,84,94,96,101,105,106,[118][119][120][121]126 with CPSS because galactose from milk bypasses the liver. The overall prevalence is close to 1:30,000 births and the prevalence of permanent CPSS can be estimated at 1:50,000.…”

“…Other complications have been reported in a few children that might be consequences of the CPSS: They include heart failure, 7,32,48,84,118 membranoproliferative glomerulopathy, 45,118,131,135 hypoglycemia, 53,55,77,134 hyperandrogenism, 43,52 pancreatitis, 101 rectal or vaginal bleeding, 43,67,105,132 autoimmune diseases, 64,77,99,101 protein-losing gastropathy, 35,132 unforeseen bleeding during surgery for scoliosis, 117 and acute lethal liver failure during an episode of gastroenteritis in a 1.7-year-old boy with an extrahepatic shunt. 54 Hypoxemia due to pulmonary arteriovenous shunting, pulmonary artery hypertension, encephalopathy with hyperammonemia, and glomerulopathy are known complications of cirrhosis, and their occurrence in children with congenital portosystemic shunts and minimal liver histologic lesions argues in support of the major role of communications between the portal blood and the systemic circulation in the origin of these conditions.…”

Transient Hepatic Nodular Lesions Associated with Patent Ductus Venosus in Preterm Infants

“…If the shunt rate is more than 30%, all the subsequent conditions can be found: hypergalactosemia-hyperbilirubinemia-hyperammonemia, [2][3][4]8,9 decreased Fisher's ratio of branchedchain to aromatic amino acids, 3 elevated bile acids, 3,[8][9][10] liver dysfunction, 2,4,8-10 autoimmune disorders, 10 hepatopulmonary syndrome, 2,10 and hepatic tumorlike lesions. [2][3][4] If the shunt rises more than 60%, hepatic encephalopathy can occur. 9 Analysis of families with DV have disclosed some typical pathological findings also in apparently asymptomatic younger siblings.…”

“…There is a broad spectrum from benign to malign hepatic lesions, whereby focal nodular hyperplasia (FNH) is the most frequent regenerative lesion in the portocaval shunt type. [2][3][4][5]11 Based on animal experiences, lack of portal flow and therefore decreased nutritive contribution (insulin, glucagons) could affect development, function, and regenerative capability of the liver. 11 Another response of hepatocyte to the disrupted portal flow is the evolution toward fatty degeneration.…”

“…Tumorlike hepatic lesions were reported in association with congenital and acquired portosystemic shunts, others than DV, in children and adults. There are few reports of hepatic lesions associated with DV patency in adolescents, [2][3][4] and none in preterm neonates. We recently encountered two low-birth-weight preterm infants with DV complicated by transient hepatic nodular lesions of fourth (IV) segment.…”