A 55-year-old male patient with superior vena cava (SVC) obstruction secondary to a mediastinal mass is scheduled for bronchoscopy and mediastinoscopy. The patient weighs 120 kg (250 lb) and has obvious swelling of the face, neck, and upper extremities. The tongue is large (Mallampati Classification IV) and the oral mucosa is plethoric. He is unable to lie flat, but is not dyspneic in the sitting position.

What Is the Pertinent Pathophysiology in SVC Syndrome?

The left and right subclavian and internal jugular veins join to form the brachiocephalic (innominate) veins, which in turn join to form the SVC. Venous drainage from the head and upper extremities then finds its final conduit to the heart in this large, but easily compressible, vessel. Extensive collaterals with the SVC include the azygos, the mammary, vertebral, lateral thoracic, paraspinous, and esophageal veins. The largest of these, the azygos vein, is formed from the junction of the right subcostal and the right ascending lumbar veins. It ascends in the posterior mediastinum and then passes anteriorly over the right mainstem bronchus to join the SVC as the latter enters into the right atrium. Here, the area is anatomically crowded with lymph nodes, the pulmonary artery, and the tracheobronchial structures hemmed in by the sternum anteriorly. The low-pressure SVC can be obstructed, either indirectly by external compression from vascular structures, tumor, or enlarged lymph nodes or directly by primary or secondary intraluminal thrombus or tumor (Figures 40–1 and 40–2).

Obstruction of the SVC will result in upper body venous hypertension, which forces blood to seek an alternate pathway to the heart via the previously described collateral vessels and the inferior vena cava. This upper body venous hypertension results in the classic clinical signs and symptoms of the syndrome. These include facial, neck, and arm swelling, as well as engorgement of the mucous membranes, including those of the upper airway. In some patients, it may result in laryngeal or cerebral edema, predisposing to an increased risk of surgical bleeding.

Most cases of SVC syndrome are due to extrinsic tumor compression from bronchogenic carcinoma or non-Hodgkin’s lymphoma occurring in the right paratracheal space or right pulmonary hilum.¹ From even a cursory glance at the anatomy, it is clear that the disease process may also compromise other major structures in the area, such as the pulmonary arteries, the right heart, and the tracheobronchial tree. With these factors in mind, the practitioner will want to determine the degree to which major structures are involved prior to embarking on induction of general anesthesia (GA).

What Evidence of Airway Compromise May be Apparent on History and Physical Examination?

Airway compression may be heralded by cough, dyspnea, hemoptysis, and a history of recurrent pulmonary infection. A change in voice may be due to recurrent laryngeal nerve involvement or vocal cord edema. Dyspnea, often with a history of syncope, may not necessarily be due to airway compromise but secondary to right ventricular outflow tract or right heart compression.¹

In this patient, the tongue is large, perhaps as a result of upper body venous hypertension, and the mucous membranes are plethoric, suggesting that the mucous membranes of the larynx in general, and glottis in particular, may also be engorged, edematous, and friable.

What Investigations Should be Done to Assess the Airway of the Patient?

Smaller precarinal and left paratracheal tumors may not be evident, but information about the size and location of the majority of mediastinal tumors can be obtained from chest radiography. Pulmonary function tests may be useful in predicting postoperative respiratory complications. In a recent prospective study, Bechard et al.² found a 10-fold increase in postoperative respiratory complications (pneumonia, airway edema, and atelectasis) in patients with a preoperative peak expiratory flow rate (PEFR) of less than 40% of predicted. In the same study, however, PEFR was not predictive of airway collapse. Flow-volume loops, in the supine and upright position, have been advocated to assess the degree of airway obstruction as it relates to body position and to distinguish variable from fixed intrathoracic lesions.³ However, Narang et al.¹ documented that the respiratory embarrassment caused by mediastinal masses tends to be characteristic of a fixed lesion causing predominantly inspiratory impairment.

Recent contrast-enhanced CT or MRI imaging is the most useful of all investigations in defining the relation of the mass to the other mediastinal structures. The CT or MRI can provide the practitioner with the necessary information with regard to the presence of pericardial effusion, the degree of anatomic compression of the airway, and the degree to which structures, such as the pulmonary arteries, right ventricular outflow tract, and the heart, may be compromised (Figures 40–3 and 40–4A). Transthoracic echocardiography (TTE) is useful in assessing the presence of pericardial effusion and the dynamic effects of tumor mass on the heart and great vessels. Significant pericardial effusion can result in cardiovascular collapse on induction of GA and positive pressure ventilation.

In this patient, chest CT findings were consistent with SVC obstruction. There was no evidence of pulmonary artery, right ventricular outflow tract, and myocardial or tracheobronchial compromise, and no evidence of pericardial effusion.

What Complications Are Associated with Mediastinal Masses and GA?

Most practitioners have a heightened sense of awareness when they are confronted with the patient with a mediastinal mass scheduled for surgery. We have all heard of the reports of airway obstruction or cardiovascular collapse.^4,5 We may even be familiar with the anesthesia management dogmas associated with these cases. Much of the literature documenting these catastrophic scenarios, however, involves pediatric populations.⁶ Furthermore, it is clear that one cannot extrapolate what may happen in the adult patient from the pediatric literature. The situation is further complicated by the fact that many of the sickest patients, like those with SVC syndrome, are managed with chemotherapy or radiation to shrink their tumors prior to presenting for surgery and GA (Figure 40–4A and B), or they are managed with less invasive surgical techniques not requiring GA. Confusing the picture even more is the fact that some series include small or posterior mediastinal masses that are unlikely to be associated with significant cardiorespiratory compromise.²

The only studies that have evaluated the incidence of life-threatening cardiorespiratory compromise are those by Azarow et al.⁶ and Bechard et al.² Azarow et al.⁶ noted that there was a significant difference in anesthetic risk between adults and children with mediastinal masses undergoing GA. The authors noted that although the mortality in both groups was similar, mortality in the pediatric group is primarily related to perioperative respiratory complications whereas mortality in the adult group is due to the malignancy itself.⁷ Total airway obstruction in pediatric patients during GA has been associated with preoperative tracheal compression of more than 50%.⁷ Significant airway compromise in the adult, concomitant with GA, however appears to be a rare event. In Bechard et al.’s² prospective study of 98 adult patients, there was no intraoperative airway obstruction in any of the eight patients with preoperative airway compression >50% and there have only been four case reports of marked airway compromise in the adult literature.^8–11 Caution in interpreting these results, however, is warranted. In Bechard et al.’s study, GA was avoided in eight patients deemed to be high risk based on symptoms and radiological findings including mass size, tracheal compression, and pericardial effusion. It is not inconceivable that the prudent practitioner may consider GA contraindicated in patients with similar pathology.

Tracheal compression greater than 50% in the adult population was, however, associated with a sevenfold increase in respiratory complications, but these were related to pneumonia, airway edema, and atelectasis in the first 48 hours postoperatively.²

Whether the patient exhibits signs and symptoms related to the mediastinal mass effect seems to be important. A study by Hnatiuk et al.¹² suggested that symptomatic patients were more likely to experience complications, and Bechard et al.² identified stridor, orthopnea, cyanosis, jugular distension, and SVC syndrome as factors associated with perioperative complications. In Bechard et al.’s² study, 3 of 105 anesthetics were complicated by severe cardiovascular compromise; two of which were associated with pericardial effusion. There have been reports of severe airway obstruction occurring in asymptomatic patients, but again this seems limited to the pediatric population.² The one exception being an asymptomatic 19-year-old male, with an anterior mediastinal mass, breathing spontaneously through a 7.5-mm ID Univent endotracheal tube who suffered right mainstem bronchial collapse following introduction of a flexible bronchoscope (FB).¹¹