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Management of Innominate Vein Rupture During Superior Vena Cava Angioplasty

Kuhn, Joseph DO, PharmD*; Kilic, Ahmet MD; Stein, Erica MD*

doi: 10.1213/XAA.0000000000000354
Case Reports: Case Report

Although vessel perforation rarely occurs during percutaneous transluminal angioplasty of a central venous stenosis, it can be a rapidly fatal complication when accompanied by pericardial tamponade. The present case report details our experience with this dangerous complication. It also highlights the risk factors for and the pathogenesis of central venous stenosis, the clinical findings associated with inadvertent vessel perforation during an intervention, and anesthetic management strategies for pericardial tamponade resulting from vessel perforation.

From the *Department of Anesthesiology, Ohio State University Medical Center, Columbus, Ohio; and Department of Cardiothoracic Surgery, Ohio State University Medical Center, Columbus, Ohio.

Accepted for publication March 22, 2016.

Funding: None.

The authors declare no conflicts of interest.

Address correspondence to Joseph Kuhn, DO, PharmD, Department of Anesthesiology, Ohio State Wexner Medical Center, 410 W 10th Ave, Doan Hall N 411, Columbus, OH 43210. Address e-mail to

The incidence of nonmalignant/noninfectious central venous obstruction and stenosis, specifically of the superior vena cava (SVC), has increased during the past 3 decades; this increase is thought to reflect the increasing use of chronic indwelling IV devices.1 Because the placement of central venous catheters has been shown to result in a high incidence of central venous obstruction and stenosis, patients undergoing hemodialysis are considered at high risk for this complication.1 First-line treatment of obstructions in this patient population includes the use of percutaneous transluminal angioplasty (PTA), which has been found to be a successful and safe treatment option. However, rupture and perforation of the vessel are rare but serious complications of this procedure. We present a case in which innominate vein rupture occurred during routine recanalization, requiring open surgical repair.

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The patient reviewed the details of this case report and gave his written permission for its publication.

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A 32-year-old man (177 cm, 100 kg) with a medical history that included end-stage renal disease because of poststreptococcal glomerulonephritis and congenital left-sided atrophic kidney as well as obstructive sleep apnea presented for percutaneous SVC angioplasty and placement of a tunneled hemodialysis catheter in the left internal jugular vein. The patient also had a history of failed arteriovenous fistulas and grafts of both upper extremities and central venous obstructions of the right internal jugular vein, right subclavian vein, bilateral innominate veins, and SVC. He was currently undergoing hemodialysis via a left femoral catheter. A recent myocardial stress perfusion scan result was negative for ischemia and showed an ejection fraction of 64%, normal right ventricular function, and no significant valvular disease. Preoperative laboratory results, including those for potassium and coagulation parameters, were within normal limits.

The patient was taken to the interventional radiology suite, where standard American Society of Anesthesiologists monitors were placed, and general anesthesia was induced with lidocaine (40 mg), propofol (180 mg), and succinylcholine (120 mg). After the patient underwent endotracheal intubation, general anesthesia was maintained with desflurane (5.0%–5.8%). The patient required intermittent boluses of phenylephrine and vasopressin for mild hypotension (mean arterial blood pressure [MAP], 40–50 mm Hg), necessitating a phenylephrine drip (0.2–0.4 μg/kg/min) to maintain an MAP of >65 mm Hg before the start of the procedure. After the basilic vein was accessed, a vascular sheath was placed, and venography confirmed complete SVC occlusion. The left femoral hemodialysis catheter was exchanged for a vascular sheath, which was advanced into the right atrium. A wire was used to traverse the SVC occlusion. A high-pressure balloon was advanced through the basilic sheath and inflated in the area of the SVC obstruction. Upon deflation of the balloon, the patient became progressively bradycardic and hypotensive, which coincided with a decrease in end-tidal carbon dioxide, as shown by capnography. A pulse could not be palpated; therefore, chest compressions and standard advanced cardiac life support protocols were initiated for pulseless electrical activity arrest. Fluoroscopy showed contrast extravasation from the lower aspect of the SVC into the pericardium (Figure 1). The balloon was reinflated to tamponade the suspected vascular defect. Pericardial tamponade was suspected, and transthoracic echocardiogram confirmed a moderate pericardial effusion. A temporary pericardial drain was placed using ultrasound guidance, and 40 to 60 mL blood was removed. After 14 minutes of cardiopulmonary resuscitation, the patient regained perfusion with a blood pressure of 175/120 mm Hg, a heart rate of 105 beats/min, and an pulse oximetry of 98%. A femoral arterial line was placed for invasive blood pressure monitoring. To maintain sufficient blood pressure (MAP >65 mm Hg), administration of IV fluids was continued, and a norepinephrine infusion (0.025–0.1 μg/kg/min) was begun. The radiologist then decided to deflate the balloon to assess for recurrent extravasation of contrast. When the balloon was deflated under fluoroscopic guidance, the patient immediately became hypotensive, and contrast was seen accumulating in the pericardial space. The balloon was reinflated, and the patient regained hemodynamic stability. The Cardiothoracic Surgery Division was contacted, and the decision was made to take the patient to the operating room (OR) for emergent open repair.

Figure 1.

Figure 1.

Figure 2.

Figure 2.

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.

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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.

Conducting a PubMed® search through October 2015 using keywords “superior vena cava rupture,” “hemopericardium,” “central venous stenosis,” and “angioplasty,” 15 case reports describing 18 cases of SVC rupture during balloon angioplasty/stent placement were found (Table).5–19 In 10 of the cases, the SVC rupture occurred intraoperatively, resulting in 3 deaths. In the remaining 8 cases, rupture occurred some time between the immediate postoperative period and 6 months after the intervention; all of these postoperative ruptures were related to stent use and resulted in 4 deaths. Thus, the overall mortality rate for these cases was 38.9% (7 of 18). However, in patients with postoperative rupture, the mortality rate was 50% (4 of 8) compared with 30% (3 of 10) with intraoperative rupture. Eleven of the 18 cases of SVC rupture in the literature occurred in the setting of malignant occlusion; and of these 11 cases, 7 patients had undergone treatment with chemotherapy and/or radiation. Although a history of chemotherapy/radiation may appear to increase the risk of vessel perforation, the low incidence of SVC rupture necessitates further study and reporting to determine specific risk factors. However, because the reported mortality of SVC rupture is high, it is prudent to be prepared for vessel rupture by preoperatively assessing for a history of malignant stenosis, previous treatment with chemotherapy/radiation, patient willingness to accept blood products, and to schedule the case in a facility where conversion to open repair would be possible. Routine scheduling of these cases in a hybrid OR does not seem warranted because of the low incidence of vessel rupture. However, the anesthesiologist needs to be vigilant for hemodynamic changes during PTA with increased suspicion for SVC rupture if hemodynamic instability occurs.



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.

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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.

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