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J Thorac Cardiovasc Surg 2007;133:1105-1106
© 2007 The American Association for Thoracic Surgery
Brief Communication |
a Department of Thoracic Surgery, European Institute of Oncology, Milan, Italy
b Department of Anesthesia, European Institute of Oncology, Milan, Italy
c School of Medicine, University of Milan, Milan, Italy.
Received for publication October 31, 2006; accepted for publication November 28, 2006. * Address for reprints: Francesco Leo, MD, Thoracic Surgery Department, European Institute of Oncology, Via Ripamonti 435, 20100 Milan, Italy. (Email: francesco.leo{at}ieo.it).
Prosthetic replacement of the superior vena cava (SVC) has been shown to be a feasible and safe technique in the surgical treatment of selected mediastinal and lung tumors.1-3
SVC crossclamping is the most utilized technique for reconstruction of the vessel but it causes intraoperative hypotension that can be severe in some instances. The aim of this study was (1) to evaluate the incidence of hemodynamic instability during SVC crossclamping, (2) to evaluate the clinical impact on the postoperative period, and (3) to search for factors influencing its occurrence.
Since January 2002, all hemodynamic data concerning patients who had prosthetic SVC replacement at the Thoracic Surgery Department of the European Institute of Oncology were prospectively recorded during surgery with a dedicated software. Severe hemodynamic instability during SVC crossclamping was defined as any hypotension requiring (1) rapid colloids infusion (500 mL/15 min), (2) additional administration of vasoactive agents, (3) suspension of SVC clamping. Intraoperative fluid administration was managed to obtain a mean systemic pressure >80 mm Hg at SVC crossclamping, reducing the risk of cerebral edema.4 Patients received 15 to 25 mL · kg–1 · h–1 of crystalloids; if the mean systemic pressure of 80 mm Hg was not reached before SVC crossclamping, 2 mg etilephrine bolus was repeated every 5 minutes up to 3 times; if that was ineffective, a continuous infusion of dopamine 5
· kg–1 · min–1 was started and then adjusted. Before SVC clamping, heparin 5000 U was administered.
Several variables were investigated as possible predictive factors of intraoperative severe hemodynamic instability: age, sex, antihypertensive therapy, preexisting SVC obstruction, need of azygos vein clamping, duration of SVC crossclamping, decubitus (lateral versus supine), amount of fluid infusion before SVC crossclamping.
The study population was composed of 22 patients (15 men and 7 women, mean age 58.8 ± 8.2 years) who had SVC replacement from January 2002 to February 2006.
Fifteen patients had non–small cell lung cancer invading SVC, 6 patients had a thymic tumor infiltrating SVC or innominate vein or both, 1 patient had a metastatic lesion from a leiomyosarcoma infiltrating the apex of the chest. Symptoms of SVC syndrome or signs of collateral venous circulation were present in 7 patients. In 12 cases, SVC resection was performed through a muscle-sparing right thoracotomy and in 10 cases, through a sternotomy or a sternothoracotomy (hemiclamshell). Overall median SVC clamping time was 33 minutes.
Six patients (27.2%) developed severe hemodynamic instability at the time of SVC crossclamping. In 2 cases, hemodynamic instability required SVC clamp removal. In 1 case, instability was due to the clamp position, which was too close to the right atrium. Repositioning of the clamp more distally allowed SVC clamping time of 53 minutes without further instability. In the other case, the patient did not tolerate SVC crossclamping, and the reconstruction was performed with tangential SVC clamping with an infiltrated resection margin on frozen section. Hypotension was managed by fluid rapid infusion in all patients; 3 patients required additional vasoactive agents (epinephrine in 2 cases and dopamine infusion in 1 case). A satisfactory mean pressure was obtained within 6 minutes from SVC clamping in all the cases. Six hours after awakening, Glasgow scale was 15 in all patients.
All 6 patients who developed hemodynamic instability had concomitant definitive or temporary closure of the azygous vein (P = .04) and received more fluids before crossclamping as compared with stable patients (median 65.5 mL/kg vs 21.9 mL/kg, P = .03). Four patients were on antihypertensive therapy (angiotensin-converting enzyme inhibitors in 2 cases, angiotensin II receptor blockers in 2 cases; P = .04), which was stopped 24 hours before surgery.
Multivariate analysis confirmed the role of azygous vein clamping (odds ratio 2.2) and preoperative antihypertensive treatment (odds ratio 2.5) in determining intraoperative hemodynamic instability.
Results from this study showed that SVC crossclamping causes a major hypotensive response in about 30% of cases. Its management is difficult because central venous pressure is not a reliable indicator of left ventricle filling during SVC occlusion. Moreover, most patients having SVC replacement are also candidates for extensive and time-demanding lung resections (pneumonectomy or tracheal sleeve pneumonectomy) in which fluid overload is a well-known risk factor for acute respiratory distress syndrome. Therefore, fluid implementation required to maintain intracranial arteriovenous gradient during SVC crossclamping may become detrimental after subsequent pneumonectomy. For this reason, intraoperative monitoring by transesophageal echocardiography is advised in these cases.5
The hypotensive response at SVC clamping may be anticipated in some cases. In our series, 66% of patients hemodynamically instable at SVC clamping had preoperative antihypertensive treatment with angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers; treatment was stopped 24 hours before surgery. Vasoplegia induced by these drugs makes patients more sensitive to anesthesia-induced hypotension, which is further impaired by SVC clamping. An indirect confirmation of the supposed vasoplegic mechanism is the amount of fluid administered before clamping, which can represent an intraoperative test to predict hypotension at SVC closure. When more than 40 mL/kg of crystalloids or additional vasoactive agents are required to maintain a mean pressure of more than 80 mm Hg before SVC closure, a hypotensive response at clamping is more likely. As a direct consequence, it would be probably more logical to stop these drugs earlier, according to their half-life time.
Another factor to be considered is the need of concomitant azygous vein clamping, as permeability of the azygous vein is important in case of SVC closure.6 In patients without preexisting SVC obstruction, azygous flow may become crucial to maintain an adequate right filling volume during crossclamping.
In conclusion, hemodynamic instability at SVC clamping represents a frequent and transitory intraoperative problem that can be managed in almost all cases with aggressive resuscitation maneuvers. It can be anticipated when patients are on antihypertensive treatment with angiotensin system inhibitors and when a synchronous clamping of SVC and azygous vein is needed. Intraoperative hypotension by itself should not stop the operation unless corrective maneuvers are unsuccessful (5% of cases), considering that no patient from our series had direct adverse consequence from hypotension postoperatively.
References
This article has been cited by other articles:
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  J. Y. Perentes, C. C. Erling, H.-B. Ris, J.-M. Corpataux, and L. Magnusson A simple bypass technique for superior vena cava reconstruction Interact CardioVasc Thorac Surg, January 1, 2011; 12(1): 15 - 19. [Abstract] [Full Text] [PDF]
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 F. Leo and L. Spaggiari Reply to the editor. J. Thorac. Cardiovasc. Surg., October 1, 2007; 134(4): 1098 - 1098. [Full Text] [PDF]
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C. Rossella and S. Nazari Superior vena cava resection without blood flow interruption. J. Thorac. Cardiovasc. Surg., October 1, 2007; 134(4): 1097 - 1098. [Full Text] [PDF]
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