The patient was transported to the OR with the high-pressure balloon inflated and remained hemodynamically stable throughout transport. Once in the OR, general anesthesia was maintained with isoflurane (0.8%–1.0%). The patient remained stable, and vasopressor support was discontinued. A sternotomy was performed, and upon opening the pericardium, a dense clot and scant bleeding were noted. The innominate vein was found to have a 4-cm tear through which the high-pressure balloon was seen protruding with resultant puncture of the right atrium (Figure 2). Cardiopulmonary bypass was instituted, and then a bovine pericardial patch was used to repair the innominate vein, and sutures were used to repair the right atrium. The patient was separated from cardiopulmonary bypass without the use of vasoactive medications. Protamine was administered to reverse heparinization, yet the patient remained coagulopathic. Therefore, the patient was transfused with 1 unit of platelets and 1 unit of cryoprecipitate, resulting in normalization of the ROTEM® parameters (Tem Group, Basel, Switzerland). The basilic sheath was removed, and the femoral sheath was exchanged for a temporary hemodialysis catheter. The patient was transported to the intensive care unit and was tracheally extubated the next morning. There were no anesthetic complications, and the patient had no undesired recall of intraoperative events. He was discharged on postoperative day 8.
Historically, SVC stenosis was largely a consequence of either infectious or malignant etiologies. Beginning in the 1980s, the incidence of central venous stenosis (CVS) because of noninfectious/nonmalignant causes began to increase; these cases currently account for approximately 35% of all CVS cases.1 The increase in CVS cases is thought to be attributed largely to the increased use of chronic indwelling medical devices, including catheters and pacemakers. Patients who undergo hemodialysis are at high risk for CVS for 2 reasons: (1) the direct trauma of repeated central venous cannulation/placement of indwelling catheters; and (2) the turbulent/high-velocity flows associated with dialysis and peripheral arteriovenous fistulas, resulting in endothelial damage with subsequent stenosis/obstruction.2 In patients undergoing hemodialysis, the incidence of CVS is reported to vary from 2% to 29%.3 First-line management of CVS in patients undergoing hemodialysis includes PTA with or without stent placement because surgical correction is associated with significantly increased morbidity. The success rate of PTA is estimated to be 70% to 90%, and long-term efficacy depends on the elastic quality of the lesion.4 PTA with and without stent placement is safe with a reported complication rate of only 3.9%.5 Of these complications, central venous rupture and hemopericardium remain rare occurrences.
The most important step in the management of vascular rupture during central venous angioplasty is rapid diagnosis and communication with the proceduralist. Acute onset of hemodynamic instability was a consistent presenting symptom of intraoperative vascular rupture in reported cases. In our case, with the patient under general anesthesia, we were able to notice the loss of end-tidal carbon dioxide coinciding with the onset of hypotension. The differential diagnoses of hemodynamic instability during central venous PTA include pulmonary embolism and vascular perforation. The immediate availability of fluoroscopy allows the proceduralist to rapidly identify vascular perforation with the extravasation of dye from the vascular lumen. The second most important step is control of hemorrhage and alleviating tamponade physiology, if present. Samuels et al11 outlined a stepwise algorithm when dealing with vascular perforation and advocate for the deployment of a wall stent when perforation is identified before the placement of a pericardial drain. However, our case outlines the importance of using the inflated balloon to rapidly mitigate hemorrhage while pericardiocentesis is performed. Another important step in management is timely communication with the cardiothoracic surgical team to allow for quick transition to open repair, if indicated; however, a current literature review showed that only 20% (2 of 10) intraoperative vascular perforations required surgical repair.
Although pharmacologic interventions can prevent hemodynamic compromise with clinically significant pericardial tamponade, timely drainage and treatment of the underlying cause of tamponade are ultimately required. In the case described here, open repair was necessary to control the bleeding. Because the initial vascular injury resulted in complete hemodynamic collapse, it is unlikely that the patient would have remained stable for transport to the OR without the high-pressure balloon occluding the vascular tear. Therefore, if the high-pressure balloon occludes the vascular tear, the anesthesiologist and proceduralist should have a low threshold for keeping the endovascular balloon inflated because it may promote hemodynamic stability during the transition to permanent repair. Early and effective communication among the radiology, surgery, and anesthesiology teams allowed for a safe transition to the OR for definitive repair.
Percutaneous angioplasty and/or stenting for the treatment of CVS has been shown to have a low rate of associated complications. However, because the mortality rate associated with vascular rupture can be high, triage of high-risk patients, prompt recognition, and treatment of acute pericardial tamponade are necessary. Reinflation of the endovascular balloon should be used to mitigate bleeding, if feasible, followed by timely evacuation of the pericardial effusion.
1. Wilson LD, Detterbeck FC, Yahalom J. Clinical practice. Superior vena cava syndrome with malignant causes. N Engl J Med 2007;356:18629.
2. Collin G, Jones RG, Willis AP. Central venous obstruction in the thorax. Clin Radiol 2015;70:65460.
3. Mansour M, Kamper L, Altenburg A, Haage P. Radiological central vein treatment in vascular access. J Vasc Access 2008;9:85101.
4. Kundu S. Central venous obstruction management. Semin Intervent Radiol 2009;26:11521.
5. Siani A, Marcucci G, Accrocca F, Antonelli R, Mounayergi F, Rosati MS, Gabrielli R. Endovascular central venous stenosis treatment ended with superior vena cava perforation, pericardial tamponade, and exitus. Ann Vasc Surg 2012;26:733.e912.
6. Oshima K, Takahashi T, Ishikawa S, Nagashima T, Hirai K, Morishita Y. Superior vena cava rupture caused during balloon dilation for treatment of SVC syndrome due to repetitive catheter ablation—a case report. Angiology 2006;57:2479.
7. Brown KT, Getrajdman GI. Balloon dilation of the superior vena cava (SVC) resulting in SVC rupture and pericardial tamponade: a case report and brief review. Cardiovasc Intervent Radiol 2005;28:3726.
8. Da Ines D, Chabrot P, Motreff P, Alfidja A, Cassagnes L, Filaire M, Garcier JM, Boyer L. Cardiac tamponade after malignant superior vena cava stenting: two case reports and brief review of the literature. Acta Radiol 2010;51:2569.
9. Boardman P, Ettles DF. Cardiac tamponade: a rare complication of attempted stenting in malignant superior vena caval obstruction. Clin Radiol 2000;55:6457.
10. Khalid I, Omari M, Khalid TJ, Castillo E, Khandelwal A, Kattoo R. Pericardial tamponade after superior vena cava stent: are nitinol stents safe? Asian Cardiovasc Thorac Ann 2010;18:2946.
11. Samuels LE, Nyzio JB, Entwistle JW. Superior vena cava rupture during balloon angioplasty and stent placement to relieve superior vena cava syndrome: a case report. Heart Surg Forum 2007;10:E7880.
12. Ploegmakers MJ, Rutten MJ. Fatal pericardial tamponade after superior vena cava stenting. Cardiovasc Intervent Radiol 2009;32:5859.
13. Mansour M, Altenburg A, Haage P. Successful emergency stent implantation for superior vena cava perforation during malignant stenosis venoplasty. Cardiovasc Intervent Radiol 2009;32:13126.
14. Brant J, Peebles C, Kalra P, Odurny A. Hemopericardium after superior vena cava stenting for malignant SVC obstruction: the importance of contrast-enhanced CT in the assessment of postprocedural collapse. Cardiovasc Intervent Radiol 2001;24:35355.
15. Martin M, Baumgartner I, Kolb M, Triller J, Dinkel HP. Fatal pericardial tamponade after Wallstent implantation for malignant superior vena cava syndrome. J Endovasc Ther 2002;9:6804.
16. Smith SL, Manhire AR, Clark DM. Delayed spontaneous superior vena cava perforation associated with a SVC wallstent. Cardiovasc Intervent Radiol 2001;24:2867.
17. O’Horo SK, Soares GM, Dubel GJ. Acute pericardial effusion during endovascular intervention for superior vena cava syndrome: case series and review. Semin Intervent Radiol 2007;24:826.
18. Recto MR, Bousamra M, Yeh T Jr. Late superior vena cava perforation and aortic laceration after stenting to treat superior vena cava syndrome secondary to fibrosing mediastinitis. J Invasive Cardiol 2002;14:6249.
19. Funaki B, Doshi T. Pulseless electrical activity arrest after SVC dilation. Semin Intervent Radiol 2007;24:4336.