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    Abstract
   Introduction
   Case Report
   Discussion
    References
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Table of Contents
CASE REPORT  
Year : 2013  |  Volume : 16  |  Issue : 2  |  Page : 133-136
An unusual cause of intraoperative acute superior vena cava syndrome


Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, MN

Click here for correspondence address and email

Date of Submission17-Aug-2012
Date of Acceptance13-Dec-2012
Date of Web Publication29-Mar-2013
 

   Abstract 

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.

Keywords: Acute superior vena cava syndrome, Intraoperative, Retractor

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;16:133-6

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 Sep 22];16:133-6. Available from: http://www.annals.in/text.asp?2013/16/2/133/109770



   Introduction Top


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 Top


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: Hemodynamics during intraoperative SVC syndrome. SBP = Systemic blood pressure ( redbars , top ) ; Heartrate (blue #, top); PAP = Pulmonary artery pressure (blue bars, bottom); CVP = Central venous pressure (blue scope sign, bottom)

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Figure 2: TEE bicaval view during intraoperative SVC syndrome. Mid-esophageal bicaval view at 104° demonstrating the SVC obstruction. LA: Left atrium; SVC: Superior vena cava

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Figure 3: TEE bicaval view after echo guided retractor adjustment. Mid-esophageal bicaval view at 105° demonstrating adequate SVC diameter after sternal retractor repositioning. LA: Left atrium; RA: Right atrium; SVC: Superior vena cava

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   Discussion Top


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.

 
   References Top

1.Rice TW, Rodriguez RM, Light RW. The superior vena cava syndrome: clinical characteristics and evolving etiology. Medicine 2006;85:37 - 42.  Back to cited text no. 1
    
2.Cheng S. Superior vena cava syndrome: A contemporary review of a historic disease. Cardiol Rev 2009;17:16-23.  Back to cited text no. 2
    
3.Kumar R. Iatrogenic superior vena cava syndrome during off pump CABG. Ann Cardiac Anaesth 2012;15:320-1.  Back to cited text no. 3
    
4.Parish JM, Marschke RF Jr, Dines DE, Lee RE. Etiologic considerations in superior vena cava syndrome. Mayo Clin Proc Mayo Clin 1981;56:407-13.  Back to cited text no. 4
    
5.Woodyard TC, Mellinger JD, Vann KG, Nisenbaum J. Acute superior vena cava syndrome after central venous catheter placement. Cancer 1993;71:2621-3.  Back to cited text no. 5
    
6.Wilson LD, Detterbeck FC, Yahalom J. Clinical practice. Superior vena cava syndrome with malignant causes. N Engl J Med 2007;356:1862-9.  Back to cited text no. 6
    
7.Kim HJ, Kim HS, Chung SH. CT diagnosis of superior vena cava syndrome: Importance of collateral vessels. AJR Am J Roentgenol 1993;161:539-42.  Back to cited text no. 7
    
8.Trigaux JP, Van Beers B. Thoracic collateral venous channels: Normal and pathologic CT findings. J Comput Assist Tomogr 1990;14:769-73.  Back to cited text no. 8
    
9.Plochl W, Cook DJ, Orszulak TA, Daly RC. Intracranial pressure and venous cannulation for cardiopulmonary bypass. Anesth Analg 1999;88:329-31.  Back to cited text no. 9
    
10.Chee CE, Bjarnason H, Prasad A. Superior vena cava syndrome: An increasingly frequent complication of cardiac procedures. Nat Clin Pract Cardiovasc Med 2007;4:226-30.  Back to cited text no. 10
    
11.Albacker TB, McGrath T, Gillinov MA. Superior vena cava syndrome post minimally invasive mitral valve repair. J Cardiac Surg 2010;25:174-5.  Back to cited text no. 11
    
12.Yildirim I, Dilek E, Emrah E, Yusuf U, Halit Proff V. An interesting iatrogenic superior vena cava syndrome following open-heart surgery. Paediatr Anaesth 2007;17:393-4.  Back to cited text no. 12
    
13.Algethamy H, Nicolle D, Novick R, Saito A, Young GB. Blindness with superior vena cava obstruction after cardiac surgery. Can J Neurol Sci 2010;37:897-900.  Back to cited text no. 13
    

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

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.109770

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    Figures

  [Figure 1], [Figure 2], [Figure 3]

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