FIG 70.7 Decompressing venovenous collateral (A) Anteroposterior projection and (B) lateral projection of an angiographic image taken with contrast injected into the brachiocephalic vein The image was taken 2 weeks after a superior cavopulmonary connection due progressive hypoxemia (systemic oxygen saturation 65%) The asterisk demonstrates a venovenous collateral “decompressing” the higher-pressure superior systemic venous system into the lower-pressure pulmonary venous system Temporary pacing wires are seen on the atrium and ventricle LUPV, left upper pulmonary vein See Videos 70.1 to 70.5 for results following coil embolization (Courtesy Joshua P Kanter, MD, Children's National Medical Center.) An important clinical observation during staged reconstruction has been the presence of significant hypoxemia in smaller or younger infants (e.g., less than ~4 kg or ~3 months) who undergo a superior cavopulmonary connection, frequently resulting in a longer hospital stay and increased resource utilization.76–80 During cardiac catheterization, pulmonary venous oxygen saturations are typically normal Despite the presence of significant hypoxemia and low calculations of pulmonary blood flow, significant decompressing venovenous collaterals are frequently absent on venous angiography The etiology of the decreased Qp and significant hypoxemia has thus far been unexplained Experimentally, in patients with a structurally normal heart, antegrade cerebral blood flow has been shown to remain normal over wide ranges of increased intracranial pressure, as would be expected secondary to increased pressure in the superior caval vein Therefore elevated PVR does not decrease antegrade cerebral blood flow; indeed, this has been shown in elegant studies by Fogel et al utilizing magnetic resonance imaging.81 We speculate that the decreased Qp and significant hypoxemia seen in these infants may be caused by venovenous collaterals that drain posteriorly and inferiorly from the head and neck via the cerebrospinal venous system (Fig 70.8) This paraspinal venous network is without valves and includes the Batson plexus, a network of veins thought to regulate intracranial pressure through the balance of cerebrospinal fluid production and venous drainage.82-87 Decompression of venous return away from the superior caval vein posteriorly through this system may cause reduced pulmonary blood flow; however, identification of this mechanism cannot be determined either by echocardiography or venous angiography Studies are currently under way to assess flow through the cerebrospinal circulation as a possible cause of decreased pulmonary blood flow and significant postoperative hypoxemia in these small infants with a Glenn circulation FIG 70.8 Cerebrospinal venous system (A) Redirection of cerebral venous return may occur in the early postoperative period, bypassing the pulmonary arteries to connect with lower body venous return and causing decreased pulmonary blood flow and hypoxemia (B) Venous return from the head, rather than draining through the higher pressure jugular veins and superior caval vein, drains through the basilar venous plexus, which connects with the Batson plexus—a valveless system of veins connecting the paravertebral veins inferiorly toward the pelvis (A, From Breschet G, Recherches anatomiques physiologiques et pathologiques sur le systáeme veineux Paris: Rouen fráeres; 1829 Courtesy the Sidney Tobinick collection.) Following the total cavopulmonary connection (Fontan procedure), upper- and lower-body venous pressures are equal; therefore the only pressure gradient in ... Recherches anatomiques physiologiques et pathologiques sur le systáeme veineux Paris: Rouen fráeres; 1829 Courtesy the Sidney Tobinick collection.) Following the total cavopulmonary connection (Fontan procedure), upper- and