Cannulation of a persistent left superior vena cava or a pericardiophrenic vein

To the Editor, We read with interest the recently published case report by Schreiber et al., and in our view, the diagnosis of a persistent left superior vena cava (PLSVC) is unclear. The diagnosis appears to have been based on the features seen on the anterior chest x-ray and the findings at mini-sternotomy. The differential diagnosis of a cannula observed to be passing straight down from the left internal jugular vein to the mediastinum on an anterior chest x-ray would include both extravascular and intravascular placement with intravascular siting, including intra-arterial (aortic) and intravenous (left internal thoracic, pericardiophrenic, PLSVC, and left superior intercostal veins) siting. Features that may help differentiate between the various veins include the lateral arching of the superior intercostal vein near the aortic arch in the upper mediastinum before proceeding caudally, the lateral turning of the pericardiophrenic vein lower in the mediastinum along the left heart border, and the medial turning of the PLSVC near the left atrium. A simple way to demonstrate this is to repeat the anterior chest x-ray following the injection of intravenous contrast via the cannula to outline the vessel. Schummer recommends a lateral chest x-ray with injected contrast to help determine the position of the cannula where the lateral thoracic vein lies anteriorly passing to the chest wall, the pericardiophrenic vein and PLSVC lie centrally, while the superior intercostal vein lies more posterior. The mini-sternotomy did not define the lower limit of the cannulated vessel, but it did confirm its origin at the caudal junction of the left internal jugular vein and the left subclavian vein. However, all four of the abovementioned veins could arise from this site, with the pericardiophrenic vein and the PLSVC occupying similar positions in the upper mediastinum. Although the pericardiophrenic vein is usually a small vein in patients with portal hypertension (as is the case with liver transplant patients), it may be involved with gastroesophageal varices and portosystemic shunting causing enlargement. The authors reasoned that the hemodynamic instability with the institution of veno-venous bypass (VVB) and its reversibility on clamping the VVB circuit was due to blood loss into the left pleural cavity. However, blood loss sufficient to cause such a sudden change would presumably need volume resuscitation to restore hemodynamic stability. Furthermore, no overt damage to the cannulated vessel was observed, blood could be withdrawn easily from the cannula, and the patient was stable up to the institution of VVB. At the time, transesophageal echocardiography detected a large left pleural collection; however, the chest tube was not inserted until the completion of liver transplantation and only 1 L of dark blood was drained via the chest tube. Although it is true that a dilated coronary sinus may cause left ventricular inflow tract obstruction due to its proximity to the mitral valve, the coronary sinus was not dilated on the preoperative transthoracic echocardiography. An alternative explanation could be that the cannulated vessel was a dilated pericardiophrenic vein involved in portosystemic shunting, and during VVB, blood would flow down this vessel in a retrograde manner and would not be returned to the heart. This would have caused an immediate drop in venous return, which would have been immediately reversible on clamping the VVB circuit. Blood in the left pleural cavity may have originated from several sources, including the contralateral diaphragm during surgery. A. Verniquet, MD (&) R. Kakel, MD James Paton Memorial Hospital–Central Health, Gander, NL, Canada e-mail: andrewverniquet@hotmail.com