147 - Barrett s Esophagus

Editors: Shields, Thomas W.; LoCicero, Joseph; Ponn, Ronald B.; Rusch, Valerie W.

Title: General Thoracic Surgery, 6th Edition

Copyright 2005 Lippincott Williams & Wilkins

> Table of Contents > Volume II > The Mediastinum > Section XXVIII - Mediastinal Infections, Overview of Mass Lesions in the Mediastinum, and Control of Vascular Obstructing Symptomatology > Chapter 172 - The Use of Prosthetic Grafts for the Replacement of the Superior Vena Cava

Chapter 172

The Use of Prosthetic Grafts for the Replacement of the Superior Vena Cava

Paolo Macchiarini

Philippe Dartevelle

Unlike the inferior vena cava (IVC), the resection of which has been reviewed by Beck and Lalke (1998), reconstruction of the superior vena cava (SVC) at the time of complete SVC resection is necessary to maintain the upper venous drainage and avoid fatal neurologic complications. However, with SVC graft reconstruction, significant morbidity may be involved, not only acute cerebral edema related to prolonged cross-clamping time, but also late graft thrombosis, anastomotic problems, and graft infection. This emphasizes the great attention to details required in the pre-, intra-, and postoperative management of SVC reconstruction.

SURGICAL ANATOMY

The SVC originates from the confluence of the two innominate veins at the level of the cartilaginous portion of the first right rib. It descends into the anterior portion of the visceral compartment of the mediastinum and enters the right atrium. Its trunk has an average length of 7 cm and transverse diameter of 2 cm. It is adjacent to the thymus gland and right pleura and lung anteriorly; the right lateral-tracheal lymphatic chain, pulmonary artery, and superior pulmonary vein posteriorly; the ascending aorta medially; and the right pleura, phrenic nerve, and small superior diaphragmatic vessels laterally.

The caval-atrial junction is within the pericardium. The serous pericardium englobes the anteroexternal surface of the SVC for a length of 2 cm. The sinus node is located along the anterolateral aspect of the junction between the SVC and the right atrium. It is superficial, lying just beneath the epicardial surface in the sulcus terminalis, and measures approximately 15 5 1.5 mm. The medial area lying between the intrapericardial SVC and ascending aorta includes: (a) an extrapericardial region where the origin of the right main bronchus lies, and (b) the anterior aspect of the pulmonary artery lying behind the SVC and the right orifice of the Thiele sinus.

McIntire and Sykes (1949) described four main collateral routes of the SVC in humans: (a) the azygos venous system (only collateral draining directly into the posterior surface of the SVC above the right pulmonary artery and main bronchus); (b) the internal thoracic venous system (where the blood pours into the IVC from the internal thoracic vein through the superior and inferior epigastric veins, and external and common iliac veins); (c) the vertebral venous system (where the blood from the sinus venosus and bilateral brachiocephalic veins flows into the intercostal, lumbar and sacral veins, and then pours into the IVC; portions of this blood flow into the internal thoracic veins); and (d) the external thoracic venous system (this is the superficial collateral system where the blood from the subclavian vein and the axillary vein reaches the lateral thoracic vein and then pours into the femoral vein through the thoracoepigastric and superficial epigastric veins (see Chapter 170).

Hemodynamic Considerations

The first clinical experiences with SVC surgical replacement by Jarvis and Kanar (1956), Thomas (1959), and Salsali (1966) reported almost uniformly a cerebral edema nearly 60 minutes after the interruption of the venous flow. A plausible explanation of this phenomenon was the resulting: (a) venous stasis at the level of the cephalic territory, (b) problems in the absorption capacity of the cerebral fluid, (c) cellular hypoxia and hypercapnia resulting from the vascular stasis, and (d) modification of the permeability of the cerebral vessels leading to vasogenic cerebral edema. Recently, however, we two authors and a colleague (1995) provided evidence that the hemodynamic repercussions of the SVC clamping depend on whether or not the SVC is obstructed.

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For patients whose SVC is completely obstructed or tightly stenosed, intraoperative venous clamping results in a negligible hemodynamic compromise since a functioning collateral venous network already exists and supplements the flow obstruction of the SVC. However, although Masuda and co-workers (1989) showed that 1-hour clamping of a nonobstructed SVC were well tolerated in a nonhuman primate model, we and a colleague (1995) failed to confirm this clinically. In these circumstances, venous clamping time beyond 45 minutes is badly tolerated from a clinical standpoint, and a longer period of time might induce irreversible brain damage, especially after ligation of the azygos vein (almost always necessary during total SVC replacement). The reason behind this is that the reduced return of venous blood flow to the right heart causes a cascade of hemodynamic events leading to reduced cardiac output and cerebral perfusion pressure (the safe physiologic level of which should be >60 mm Hg), as noted by McDowall (1985).

For some patients whose invaded SVC is not obstructed, even a brief venous clamping may trigger a hemodynamic cascade of events, including decreased cardiac inflow and outflow, increased pressure in the cerebral venous system, and alterations of the cerebral arteriovenous gradient, leading to irreversible brain damage and intracranial bleeding. Several technical details may mitigate this hemodynamic instability in the nonobstructed SVC (e.g. pharmacologic agents and fluid implementation, shortening the venous clamping time, and anticoagulation therapy). Intraluminal shunting of the blood from one of the brachiocephalic veins into the right atrium may reduce the hemodynamic consequences of venous clamping in animals as reported by Gonzales-Fajardo and co-workers (1994) and in humans by Warren and colleagues (1998) for at least 35 minutes; unfortunately, the mean clamping time of the SVC during an excision of the lung or of mediastinal tumors is usually longer than this period of time.

INDICATIONS AND CONTRAINDICATIONS

The SVC is usually subject to easy obstruction due to its anatomic site, thin wall, low hemodynamic pressure, and encirclement by chains of lymph nodes draining all of the (right) thoracic cavity and mediastinal tissues. The main indications and contraindications for SVC resection and reconstruction are outlined in Table 172-1. Major elective SVC reconstructive procedures should be limited to mediastinal tumors and, according to McCormack (1995), to less than 1% of operable patients with right-sided bronchial carcinomas invading the SVC directly or, as we (1998) have noted, to even a lesser extent when the invasion is the result of extension of the tumor from involved superior mediastinal lymph nodes. Palliative SVC procedures are rare and limited to slow-growing diseases like mediastinal primary or secondary fibrosis, SVC thrombosis of unknown etiology, or saccular SVC aneurysms.

Table 172-1. Indications and Contraindications for Superior Vena Cava (SVC) Replacement

Indications Contraindications
Tumors SVC syndromes related to unresectable tumors
Obstructed SVC with a rich collateral vein circulation
   Non small cell lung cancer
   Anterior mediastinal mass
   Primary SVC tumors
Abnormal venous walls of the proximal veins
Vascular   
Primary saccular aneurysms
   Primary malformations
Trauma
   Iatrogenic
   Blunt
   Penetrating

Surgery should not be performed when: (a) the cephalic venous bed is obstructed; (b) the proximal veins have abnormal venous walls as well; and (c) the SVC is chronically obstructed, since the existing well-developed collateral venous circulation competes and reduces the blood flow through the graft. In these circumstances, SVC revascularization might be performed using either a jugular or an axillary vein, but such procedures involve a reduced venous blood flow through the graft because of the preexisting collateral venous network and also require a longer prosthesis (passing subcutaneously with possible major kinkings), and therefore resulting in a higher risk for thrombosis.

PREOPERATIVE STUDIES

A clinical preoperative workup evaluating the extension of the primary disease should be performed routinely. All patients should undergo a superior vena cavography before operation to delineate the site and extension of the venous obstruction and the presence of possible proximal thrombosis, and to anticipate where the proximal graft anastomosis can be made. Echocardiography eliminates thrombotic extension into the right atrium and evaluates the patency of the jugular and axillary veins. Since a majority of patients with bronchial cancer may present with a clinically and radiologically silent SVC invasion, thoracic computed tomography (CT) (to evaluate the possible invasion of the posterior wall of the terminal portion of the SVC) and pulmonary angiography (to demonstrate possible involvement of the upper mediastinal portion of the pulmonary artery) are key diagnostic tools to anticipate the necessity of an SVC reconstruction. The brain should also be investigated by CT to assess the tolerance to the SVC cross-clamping.

INTRAOPERATIVE MONITORING

Patients should be ventilated through a double-lumen tube to obtain one-lung ventilation. Continuous arterial and

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venous pressure measurements are essential. A radial arterial line should be inserted transcutaneously to monitor the decline of the systemic pressure caused by the reduced venous return to the right heart during venous clamping. A plastic catheter is inserted into the cephalic vein in the forearm or more proximally in the antecubital fossa or into the right internal jugular vein to monitor the venous pressure in the cephalic territory. The arterial and venous lines are essential to monitor and maintain the physiological arterial-venous brain parenchymal gradient.

A Foley catheter is inserted to monitor urine output. Electrocardiographic monitoring (limb or chest limbs) should be in position to monitor cardiac electrophysiologic alterations during venous clamping, since the distal clamp may be too close to the sinus node. At least two venous lines should be placed in the lower limbs to achieve volume expansion during venous clamping. Transesophageal echography and nasogastric tube are optional. Cyanotic faces during SVC clamping can alert a naive anesthesiologist, but this complication is usually transient and completely reversible after venous unclamping. Clotting manifestations, like petechiae, may develop but are usually transient and disappear 1 to 2 weeks after the operation.

SURGICAL APPROACH

The usual approach includes a right thoracotomy in the fifth intercostal space for bronchial carcinomas and a median sternotomy for tumors originating from the anterior compartment of the mediastinum, respectively. Median sternotomy allows a large exposure of the entire anterior mediastinum, right atrium, both brachiocephalic veins, and the SVC on their entire lengths; moreover, this incision can be easily extended to the neck. The right thoracotomy yields the best exposure of the right hilum and excellent visualization of the SVC and right atrium. However, this approach renders dissection, control, and revascularization of the left brachiocephalic vein technically demanding.

Choice of Materials

The materials currently available for SVC reconstruction include autogenous venous or pericardial grafts as reviewed by Warren and co-workers (1998) and prosthetic grafts that have been described by one of us (PD) and colleagues (1991). Although autogenous grafts represent the nearest approximation of the ideal blood vessel substitute and are acknowledged to provide the best recurrent results of vascular reconstruction, it is evident that such grafts are unsuitable for large-vessel reconstruction, require intraoperative time-consuming shunting, and are likely to become compressed by the postoperative radiation-induced fibrosis.

Prosthetic grafts in the venous system are far more likely than arterial grafts to occlude, because of the relatively slow venous flow against a hydrostatic pressure gradient, low intraluminal pressure, and presence of competitive flow from venous collaterals. Not surprisingly, prosthetic replacement of the SVC usually has been regarded as an absolute surgical contraindication because of the absence of suitable graft material for reconstruction, technical fear concerning the effects of SVC clamping, graft thrombosis, and infection. However, the feasibility of reconstructing the SVC has been ameliorated by the efficacy of the presently suitable graft materials. Among them, we and a colleague (1995) provided definitive evidence that the synthetic nontextile polytetrafluoroethylene (PTFE) vascular graft (Gore-Tex, W.L. Gore & Associates, Flagstaff, AZ, U.S.A.) is the material of choice for SVC reconstruction. In effect, (a) it is the only synthetic material remaining patent in the long term; (b) shortly after its implantation, it becomes re-epithelialized with autogenous endothelial cells in human beings; and (c) its surgical implantation is associated with a negligible rate of complications. Technically speaking, (a) Gore-Tex grafts do not require preclotting, (b) do not leak, (c) are resistant to dilation in their current form, (d) are biocompatible, (e) are potentially easier to thrombectomize than vein grafts or Dacron conduits if graft thrombosis occurs, (f) are more resistant to infection, (g) have less platelet deposition and less thrombogenicity of the flow surface compared with Dacron grafts, and (h) cause substantially less complement activation and therefore leukocyte infiltration and release of inflammatory mediators. Moreover, Brewster (1995) has noted that healing at the PTFE native vessel anastomosis is stronger, resulting in a lower rate of anastomotic aneurysm formation.

Prevention of Clamping Effects

Several technical details may mitigate the hemodynamic compromise resulting from the cross-clamping of an SVC.

  • Shunt procedures. Intraluminal shunting of the blood from the innominate vein into the right atrium may reduce the hemodynamic consequences of venous clamping as suggested by Warren and colleagues (1998). Whatever the type of shunt used, their major drawbacks are their potential thrombosis and that they fill the operative field, making the performance of the distal anastomosis difficult.

  • Pharmacologic agents and fluid implementation. Such agents and fluid should increase the venous blood return to the right atrium and maintain the physiologic arteriovenous gradient in the cerebral territory. The first target is achieved by an adequate compensation of all blood losses by blood components and macromolecules. Because the cranial venous pressure may increase up to 40 mm Hg during venous clamping, maintenance of the cerebral arteriovenous gradient requires fluid administration and eventually vasoconstrictive agents.

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  • Shortening the venous clamping time. To reduce the venous clamping time, an accurate surgical strategy should be defined. For right bronchial cancers with carinal or proximal pulmonary artery invasion, it is often easier to perform the vascular step first and then the airway procedure. During the latter, all attention should be directed to avoid bacterial and tumoral contamination of the prosthesis. For mediastinal tumors involving both upper lobes, operation should be made from the left to the right side. This permits a safe and immediate revascularization between the left innominate vein and the right atrium; the right part of the excision is performed thereafter.

  • Anticoagulation therapy. Like other venous replacements, intravenous sodium heparin (0.5 mg/kg) is given before clamping, continued at a daily dose of 1 to 2 mg/kg thereafter, and switched to warfarin agents before hospital discharge.

Types of Prosthetic Superior Vena Cava Reconstruction

Segmental Replacement

Segmental replacement requires a tumor-free confluence of both innominate veins. This procedure, commonly associated with a right pneumonectomy, uses a straight, not ringed, PTFE graft (No. 18 or 20) (Fig. 172-1). After proximal (innominate veins confluence) and distal (cavoatrial junction) clampage, the invaded segment of the vein is completely excised. The proximal anastomosis between the SVC stump and the prosthesis is then performed first using a continuous 5-0 polypropylene (Prolene, Ethicon, Inc., Somerville, NJ, U.S.A.) suture started at the posterior aspect of the prosthesis in an inside to outside fashion. After its completion, the distal anastomosis is then performed in the same way. Before tightening the stretches of the distal suture, the proximal clamp is released, the prosthesis is flushed with heparinized saline solution, and any air in the graft is removed. The distal clamp is then released and the knots tied. To avoid prosthesis kinking, the length of the graft should be adapted so that the distal anastomosis rests under tension.

Revascularization from the Left Innominate Vein

This procedure, always performed through a median sternotomy, requires a ringed PTFE graft (No. 12 or 13) (Fig. 172-2). The ringed graft is imperative since after closure of the median sternotomy the prosthesis may be too long, inducing its kinking. Minimal dissection of the left innominate vein is also mandatory to avoid its rotation above the proximal anastomosis. The distal anastomosis can be performed either on the right atrium or appendage or on the inferior stump of the SVC. When the distal anastomosis is planned on the right heart, it should be performed on the right atrium because of the absence of the pectinate muscles lining the right auricle.

Fig. 172-1. Truncular superior vena cava revascularization using a synthetic, nontextile polytetrafluoroethylene vascular graft.

Revascularization from the Right Innominate Vein

Ringed grafts are preferred (No. 12 or 14) to maintain their patency and to prevent their compression by the postoperative fibrosclerosis (Fig. 172-3). The risks of kinking are minimal since the direction of the graft is almost vertical. The proximal anastomosis is not always easy to perform since the right innominate vein after its resection is often short; it has to be performed first. The distal anastomosis should be made to the SVC stump; this architecture results in the straightest and shortest graft. It is the revascularization of choice after resection of mediastinal tumors involving the origin of the SVC. Revascularization of both innominate veins should not be performed since the blood flow through each graft is lower than that observable after single revascularization.

Fig. 172-2. Revascularization between the left innominate vein and the right atrium using a synthetic, nontextile polytetrafluoroethylene vascular graft.

Fig. 172-3. Revascularization between the right innominate vein and the right atrium using a synthetic, nontextile polytetrafluoroethylene vascular graft.

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COMPLICATIONS OF SUPERIOR VENA CAVA REVASCULARIZATION

Several complications might be associated with SVC revascularization.

Anastomotic Stenosis

Superior vena cava revascularization requires a perfect technical performance, and postoperative angiographic control should be routinely performed to correct eventual anastomotic technical failures. Because the vein usually incorporates the graft on its entire transverse diameter, a stenosis at the level of the proximal anastomosis is almost impossible to observe. By contrast, an anastomotic stenosis is more commonly related to an intraoperative excessive dissection of the vein proximal to the anastomosis, which might kink, rotate, or become involved by fibrotic tissue after performance of the prosthetic-venous anastomosis. When excessive venous length or rotation are postoperatively diagnosed, surgical correction is advised. By contrast, a stenosis induced by a fibrosis may be corrected with angioplastic dilation or by use of an intraluminal stent.

Graft Thrombosis

Thrombosis usually represents an early postoperative complication, the causes of which are technical pitfalls or an inappropriate indication (implantation on a recanalized vein with major pathologic venous wall sequelae, insufficient proximal vein bed, or a chronic SVC syndrome associated with a very developed venous collateral circulation that competes with the blood flow through the graft). The major consequences of graft thrombosis are an acute clinical SVC syndrome leading to irreversible brain damage and passage and lodgment of thrombotic clots into the pulmonary circulation. My colleagues and I have never observed secondary graft thrombosis in our patients, even after discontinuation of anticoagulation therapy.

Graft Infection

Graft infection is a serious risk inherent to all prosthetic vascular replacements and more likely to develop when the airway is opened, a bronchial suture and lung parenchymal resections are performed, and when the surgical procedure is performed after induction radiation/chemotherapy. Infection can manifest itself by a mediastinitis, a thoracic empyema, or septicemia as in infected thrombophlebitis. Treatment depends on the presence or absence of a systemic septicemia. In the absence of severe septic syndrome, the prosthesis might be conserved by using an omentoplasty covering the graft. On the contrary, septicemia or severe

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septic syndrome necessitates graft excision, which may be badly tolerated when the graft is patent.

COMMENTS

Patients most suitable for elective SVC prosthetic reconstruction are limited to those with operable anterior mediastinal tumors or right-sided bronchial carcinomas without hemodynamically significant venous outflow obstruction. The caval reconstruction requires great technical expertise and although it likely adds significant procedural time, the long-term survival and patency of SVC prosthetic reconstruction appears to exceed the related morbidity and operative mortality.

REFERENCES

Beck SD, Lalke SG: Long-term results after inferior vena caval resection during retroperitoneal lymphadenectomy for metastatic germ cell cancer. J Vasc Surg 28:808, 1998.

Brewster DC: Prosthetic grafts. In Rutheford RB (ed): Vascular Surgery. Philadelphia: WB Saunders, 1995.

Dartevelle P, et al: Long-term follow-up after prosthetic replacement of the superior vena cava combined with resection of mediastinal-pulmonary malignant tumors. J Thorac Cardiovasc Surg 102:259, 1991.

Dartevelle P, Macchiarini P, Chapelier A: Superior vena cava resection and reconstruction. Chest Surg Clin North Am 5:345, 1995.

Gonzales-Fajardo JA, et al: Hemodynamic and cerebral repercussions arising from surgical interruption of the superior vena cava. Experimental model. J Thorac Cardiovasc Surg 107:1044, 1994.

Jarvis FJ, Kanar EA: Physiologic changes following obstruction of the superior vena cava. J Thorac Cardiovasc Surg 27:213, 1956.

Macchiarini P, Dartevelle P: Extended resections for lung cancer. In Roth JA, Hong WK, Cox JD (eds): Lung Cancer. 2nd Ed. Cambridge, MA: Blackwell Scientific, 1998.

Masuda H, Ogata T, Kikuchi K: Physiological changes during temporary occlusion of the superior vena cava in cynomolgus monkeys. Ann Thorac Surg 47:890, 1989.

McCormack PM: Extended pulmonary resections. In: Thoracic Surgery. New York: Churchill Livingstone, 1995.

McDowall DG: Induced hypotension and brain ischemia. Br J Anaesth 57: 110, 1985.

McIntire FT, Sykes EM Jr: Obstruction of the superior vena cava: a review of the literature and report of two personal cases. Ann Intern Med 30: 925, 1949.

Salsali M: A safe technique for resection of the nonobstructed superior vena cava. Surg Gynecol Obstet 123:92, 1966.

Thomas CP: Conservative and extensive resection for carcinoma of the lung. Ann R Coll Surg Engl 24:345, 1959.

Warren WH, Piccione W Jr, Faber LP: Superior vena caval reconstruction using autologous pericardium. Ann Thorac Surg 66:291, 1998.

Reading References

Inoue H, et al: Resection of the superior vena cava for primary lung cancer: 5 years' survival. Ann Thorac Surg 50:661, 1990.

Tsuchiya R, et al: Extended resection of the left atrium, great vessels, or both for lung cancer. Ann Thorac Surg 57:960, 1994.



General Thoracic Surgery. Two Volume Set. 6th Edition
General Thoracic Surgery (General Thoracic Surgery (Shields)) [2 VOLUME SET]
ISBN: 0781779820
EAN: 2147483647
Year: 2004
Pages: 203

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