Year : 2013  |  Volume : 16  |  Issue : 2  |  Page : 133--136

An unusual cause of intraoperative acute superior vena cava syndrome

Adam W Amundson, Juan N Pulido, Geoffrey L Hayward 
 Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, MN

Correspondence Address:
Adam W Amundson
200 1st St SW, Rochester, MN 55905


Acute intraoperative superior vena cava (SVC) syndrome is an exceedingly rare complication in the cardiac surgical population. We describe the case of a 71-year-old female undergoing multi-vessel coronary artery bypass grafting who developed acute intraoperative SVC syndrome following internal thoracic artery harvest retractor placement. Her symptoms included severe plethora, facial engorgement and scleral edema, which was associated with hypotension and severe elevation of central venous pressure. Transesophageal echocardiography was crucial in the diagnosis, management, and optimal retractor placement ensuring adequate SVC flow. Potential causes of intraoperative SVC syndrome are reviewed as well as management options.

How to cite this article:
Amundson AW, Pulido JN, Hayward GL. An unusual cause of intraoperative acute superior vena cava syndrome.Ann Card Anaesth 2013;16:133-136

How to cite this URL:
Amundson AW, Pulido JN, Hayward GL. An unusual cause of intraoperative acute superior vena cava syndrome. Ann Card Anaesth [serial online] 2013 [cited 2019 Oct 14 ];16:133-136
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Full Text


The growing need for chronic indwelling vascular devices has increased the occurrence of acute superior vena cava (SVC) syndrome. [1] Due to the profound physiologic and hemodynamic consequences of SVC syndrome the anesthesiologist needs to be aware of the unique features of this condition for its prompt diagnosis and management. There are few case reports describing the occurrence of acute SVC syndrome in the cardiac surgical patient population. Here we detail our experience with a unique intraoperative presentation of acute SVC syndrome, discuss other possible causes, and make recommendations for diagnosis and management of this rare but serious event. Transesophageal echocardiography (TEE) can be a valuable tool in confirming the diagnosis of SVC syndrome and directing therapy. Its use allowed the prompt relief of the SVC obstruction caused by an internal thoracic artery retractor and led to a good patient outcome.

 Case Report

A 71-year-old female was admitted for a non-ST-elevation myocardial infarction. Subsequent coronary angiogram demonstrated multi-vessel disease and the patient was scheduled for triple vessel coronary artery bypass grafting with left internal thoracic artery (LITA) and endovein harvest. The patient's co-morbidities included end-stage kidney disease on hemodialysis with a preexisting tunneled right internal jugular dialysis catheter, diabetes mellitus type 2, uncontrolled hypertension, bilateral moderate carotid artery stenosis, hypothyroidism, peripheral vascular disease, and anemia of chronic disease. Anesthetic induction was uneventful, as was the placement of a left radial arterial catheter, left internal jugular nine-french double lumen introducer with a pulmonary artery catheter, and a TEE probe. The sternum was split without complication and the LITA take down proceeded with placement of a standard LITA sternal retractor. The LITA retractor elevates the left side of the ribcage to provide adequate surgical exposure for artery dissection. Just before the sternum was split, 15 minutes prior to LITA retractor placement, central venous pressure (CVP) was 10 mmHg and systemic arterial pressure was 110/55 mmHg. During LITA retraction placement, the CVP reading was obscured due to red cell transfusion and subsequent series of thermodilution cardiac output measurements. After these maneuvers were completed, the CVP waveform was no longer distinguishable and showed a pressure of 54 mmHg [Figure 1]. As this value was being investigated, it was noted that there was both a reversal of flow in the left internal jugular fluid line and decreased pulse pressures while systemic pressures continued to decline to a nadir of 60/50 after 15 minutes. At the same time, the patient's head was observed to be engorged, plethoric, and with significant scleral edema. Acute SVC syndrome was suspected and TEE was used to establish the point of obstruction. A mid-esophageal bicaval view clearly showed complete SVC compression [Figure 2]. These findings were discussed with the surgical team, which removed the offending LITA retractor and relieved the SVC obstruction immediately. The central venous pressure then decreased, the head became noticeably less engorged and color improved. TEE guidance was then utilized for optimal retractor placement without compromising SVC diameter and flow [Figure 3]. The surgical procedure proceeded, was otherwise uneventful, and the patient was transferred to the intensive care unit postoperatively. The following day the patient was extubated without complications and subsequently discharged to home on postoperative day nine and without neurologic sequelae.{Figure 1}{Figure 2}{Figure 3}


SVC syndrome is defined by a decrease in blood flow through the SVC secondary to a point of obstruction. [2] Common symptoms of obstructed SVC flow include facial, head, and neck swelling with or without upper extremity edema. If the disease progresses, it may result in cerebral edema and optic neuropathy with symptoms of nausea, headache, blurry vision, or mental status changes. In severe cases, there is the possibility of airway collapse secondary to laryngeal edema and airway obstruction. [2] SVC syndrome is most commonly caused by mass effect, for example, by intrathoracic tumors, which usually present with a more gradual onset of symptoms. [1] However, as our case report shows, iatrogenic causes of SVC syndrome (i.e., mechanical obstruction, SVC stenosis or clot formation on central venous catheters or pacemaker wires) can manifest acutely. To our knowledge, this is only the second case reported of retractor related acute intraoperative SVC syndrome in the cardiac surgical patient population. [3] As acute intraoperative SVC syndrome is rare, effective management has not been well-established. The first and most important step in the perioperative management of acute SVC syndrome involves identifying and relieving the source of SVC obstruction. In any patient with an indwelling central venous catheter, thrombus formation or SVC stenosis must be excluded, as they are common causes of acute SVC syndrome. [4],[5] Intraoperative TEE can play an invaluable role in diagnosing the point of SVC obstruction as well as identifying the etiology. If the point of obstruction cannot be relieved, hemodynamic instability may occur as the result of a dramatic decrease in preload. Hemodynamic management and fluid resuscitation via upper central (internal jugular or subclavian) or peripheral venous catheters may prove to be ineffective due to the obstruction, and would further elevate central venous pressure. Alternative intravenous access should then be established using lower extremity veins (i.e., femoral veins), and all infusions should be transferred to these lines, thus allowing fluid and medications to reach the systemic circulation. The SVC obstruction and resultant rise in CVP and ICP can also cause a decrease in cerebral perfusion pressure and cerebral edema.

Patient positioning may play an important role when SVC syndrome is suspected as reverse trendelenberg position can aid venous drainage. Diuretics are less likely to be helpful in an acute perioperative presentation of SVC syndrome as their effects are delayed and they do not relieve the SVC obstruction. [6] Despite complete obstruction of the SVC, the azygos, hemiazygos and intercostal veins may allow for some collateral blood flow and SVC decompression. This process can be aided by the internal mammary veins (which drain to the superior and inferior epigastrics veins) and the long thoracic vein (which drains to femoral and vertebral veins). [7] However, this compensatory drainage is not effective in an acute obstruction, as it usually takes several weeks for these collaterals to make a significant impact in SVC drainage. [6],[7],[8] There have only been a few case reports of acute SVC syndrome in the cardiac surgical patient population; however, the overall incidence of non carcinogenic causes are on the rise. [1] In 2006, Rice et al., reviewed the outcome of 78 patients with SVC syndrome and noted that 22 of those cases were related to intravascular devices such as central venous catheters, automatic implantable cardioverter defibrillator or pacemaker wires. [1] As in our case, it is likely that the prescence of multiple large bore catheters in the SVC contributed to the further distruption of flow in the SVC that was primarily caused by the LITA retractor. The complete stasis of blood in the SVC especially with lines in the left and right internal jugular veins also placed the patient at increased risk of SVC thrombosis, which would further disrupt cerebral venous drainage.

A well-known complication during cardiopulmonary bypass, which can result in acute intraoperative SVC syndrome, is malposition of the SVC cannula. Poor SVC cannula position can either reduce or completely obstruct venous drainage from the upper body. [9] If not corrected, the obstructed SVC drainage will lead to increased intracranial pressure and cerebral edema while on bypass. Acute intraoperative presentations of SVC syndrome are rare, and most case reports describe diagnosing SVC obstruction postoperatively. Cheek, et al., reported a patient who on postoperative day four after an atrioventricular node ablation and implantation of a single lead pacemaker presented with dyspnea, swelling of her face, neck, and upper extremities. [10] A contrast-enhanced computed tomography (CT) diagnosed the SVC syndrome, and she was treated with fibrinolytics and mechanical thrombectomy. A follow-up venogram showed stenosis of the SVC-right atrium junction, which likely contributed to the thrombus formation. Another report describes a patient who underwent mitral valve repair and developed a hematoma at the SVC-right atrial junction that resulted in cardiac tamponade and SVC syndrome. [11] This was diagnosed on postoperative day two after the patient developed progressive dyspnea, lethargy, neck vein distention, and bluish skin discoloration confined to the head, neck, and upper body. After diagnosis, the patient was brought back to the operating room (OR) for clot evacuation and recovered without further event or residual side effects from the obstruction. Tight purse string closure after SVC cannula removal has also been reported to cause acute SVC syndrome in the case of a 3-year-old undergoing ventricular septal defect closure. [12] Due to a consistently elevated CVP in the intensive care unit (ICU) postoperatively, a TEE was performed, which showed a distended SVC. The patient was brought back to the OR for repair and was eventually discharged without sequelae. A case series by Algethamy, et al., describes two cases of SVC syndrome after cardiac surgery that resulted in optic neuropathy. One of these patients had an obstructive clot formed due to a stricture in the distal portion of the SVC and the other from scarring in the SVC-right atrial junction. [13] Both cases demonstrated bilateral swelling of the neck and head with diagnosis confirmed by CT.

To summarize, we describe an unusual cause of intraoperative acute SVC syndrome due to LITA retractor placement detected prior to cardiopulmonary bypass. Although the diagnosis was clinical, the use of TEE identified the point of obstruction and provided guidance to the surgical team for retractor repositioning. Thus, TEE was invaluable in identifying the cause of obstruction, directing therapy, and demonstating resolution of symptoms, which correlated with adequate SVC flow while allowing for appropriate surgical exposure.


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