Mediastinal Masses: Implications for Anesthesiologists

Shahar Bar-Yosef

Key Points

1. The patient with an anterior mediastinal mass who undergoes general anesthesia is at risk of developing severe perioperative complications, including complete airway obstruction, severe hypoxemia, profound hypotension, and cardiac arrest.

2. Predictors of perioperative complications in these patients include significant respiratory symptomatology at baseline, greater than 50% tracheal narrowing on CT scan, pericardial effusion, and SVC syndrome.

3. The basic tenets of anesthesia for these patients include preservation of spontaneous breathing, securing the airway beyond the point of obstruction, the ability to rapidly change the patient’s position, and preparation of options for managing emergencies, including rigid bronchoscopy, helium-oxygen gas mixture and CPB.

Case Vignette

A 15-year-old male patient complains of several weeks onset of cough and dyspnea, especially on lying flat. A chest x-ray taken to rule out pneumonia shows an anterior mediastinal mass. He has no other medical problems and takes no medications other than vitamins. Vital signs: BP 105/70, HR 95, room air SpO₂ 96% (sitting up). Laboratory studies are unremarkable except for leukocytosis and mild anemia. He is referred for a surgical biopsy of the mass.

For the anesthesia practitioner, mediastinal masses have been described as a catastrophe waiting to happen. Complete airway occlusion and cardiovascular collapse are well-recognized complications of general anesthesia in these patients, related to pressure on and compression of nearby major airways, blood vessels, the lung and the heart. Mildly symptomatic or even asymptomatic patients might develop severe airway and vascular obstruction during induction of general anesthesia, endangering the patient’s life.¹ It is important, therefore, to understand the anatomy and pathophysiology of mediastinal masses, to perform an adequate preoperative evaluation of the patient, and to formulate a clear anesthetic plan to ensure safe delivery of anesthesia.

CLINICAL ASPECTS OF MEDIASTINAL MASSES

Anatomy of the Mediastinum

The mediastinum extends from the thoracic inlet superiorly to the diaphragm inferiorly, and is bound between the left and right pleural sacs and lungs laterally, the sternum anteriorly and the vertebral column posteriorly (Figure 12–1). It is divided into the superior and inferior mediastinum by a plane passing through the sternal angle and the fourth thoracic vertebra. The inferior mediastinum is further divided into the anterior mediastinum which lays between the sternum and the heart, the middle mediastinum which includes the heart, the major airways and blood vessels and the esophagus, and the posterior mediastinum between the posterior pericardial sac and the vertebral column.² For clinical purposes, it is useful to consider any tumor that is anterior to a line drawn between the trachea and the posterior border of the heart as an anterior mediastinal tumor, as these are the tumors that tend to cause respiratory and vascular compression. In one series of 48 children with mediastinal masses undergoing surgery under general anesthesia, 48% (23 of 48) of patients had an anterior mediastinal mass, while of the 7 patients who developed complications during anesthesia, 6 (86%) had an anterior mediastinal mass.³

Pathology of Mediastinal Masses

Most mediastinal masses are neoplasms, either benign or malignant, the latter being either of primary growth or metastatic origin. In addition, abscesses, cysts, or vascular malformations can present as a mediastinal mass.⁴ Table 12–1 summarizes the most common types of mediastinal masses in children. In adults, lymphomas (both the non-Hodgkin and the Hodgkin types), thymomas, carcinomas (either primary or metastatic), and intrathoracic thyroid goiters comprise the vast majority of mediastinal masses, while developmental abnormalities, teratomas and neurogenic tumors are much rarer.⁵ While most tumor types have a predilection to specific parts of the mediastinum, a tissue biopsy is mandatory to determine the tumor type as well as its malignancy.

Table 12–1. Types of Mediastinal Masses in Children

Signs and Symptoms

Although mediastinal masses can present with systemic symptomatology specific to their biological behavior (eg, autoimmune phenomena, neurohormonal effects), for the anesthesiologist the main concern is the effect of the mass on the respiratory and cardiovascular systems. About half of all mediastinal masses are incidental findings on chest radiograph, and tumors that do present with symptoms tend to be malignant, probably because the rapid growth tends to cause more symptoms.⁴ In addition, signs and symptoms depend to a large extent on the size of the mass and its location. For example, neuroblastoma, a posterior mediastinal tumor, tends to cause systemic manifestations or neurological symptoms and only rarely respiratory distress. Children are more susceptible to severe compression because of the smaller size of their mediastinum, a larger thymus gland occupying a greater volume of the mediastinal cavity, increased collapsibility of the airways, and the smaller diameter of their airways and blood vessels. The smaller diameter also means that a relatively small reduction in the diameter will result in a relatively larger reduction of the cross-sectional area, and a greater increase in resistance to flow.

Common signs and symptoms associated with mediastinal masses are summarized in Table 12–2. The respiratory symptoms relate to pressure of the tumor on the trachea, leading to weakening of its wall (tracheomalacia), compression and narrowing of the lumen and bending of the airways. Most characteristically, symptoms are dynamic in nature, appearing mainly in the supine position or when intrathoracic pressure increases, as in expiration or while crying.

Table 12–2. Signs and Symptoms Related to a Mediastinal Mass

Cardiovascular symptoms can be caused by compression of the superior vena cava (SVC), pulmonary artery or the right ventricular outflow tract. Also, pericardial infiltration can result in either pericardial effusion and tamponade or in constrictive pericarditis. Rarely, intramyocardial tumor spread will lead to arrhythmias and decreased contractility. As with respiratory symptoms, changes in position or intrathoracic pressure (eg, a Valsalva maneuver), might induce cardiovascular symptoms such as syncope.

Some unique signs are associated with nerve involvement by the mediastinal tumor: hoarseness indicates recurrent laryngeal nerve involvement, Horner’s syndrome indicates sympathetic ganglion involvement, and elevated hemidiaphragm on chest x-ray is associated with phrenic nerve involvement.

Several mediastinal tumors can also cause systemic syndromes. Examples include myasthenia gravis (thymoma), myasthenia-like muscle weakness (Eaton-Lambert syndrome in bronchogenic carcinoma), hyperparathyroidism (parathyroid adenomas or bronchogenic carcinoma), thyrotoxicosis (goiter), paroxysmal tachycardia and hypertension (neuroblastoma or pheochromocytoma), and von Recklinghausen disease (neurofibromatosis).⁶

Surgery for Mediastinal Masses

Most patients who present for surgery with a mediastinal mass will require either a diagnostic or therapeutic procedure related to the mass. The rare patient might present for an unrelated surgery.⁷ The most common diagnostic procedures are a mediastinoscopy or mediastinotomy, though sometimes an extrathoracic lymph node biopsy can be performed. Therapeutic resection usually requires either a thoracotomy or median sternotomy.⁵

ANTERIOR MEDIASTINAL MASSES—ANESTHETIC ASPECTS

Pathophysiology of Perioperative Complications

Perioperative tracheobronchial compression with complete inability to ventilate is the most feared complication of anesthesia in a patient with a mediastinal mass. This has been described during induction of anesthesia as well as during emergence or even postoperatively.¹ While direct compression by the tumor is the more common mechanism for airway obstruction, in some patients bronchial compression has been linked to a mediastinal shift resulting from either severe atelectasis or lobar emphysema from a ball-valve type of obstruction.⁸ Several physiological changes that occur during anesthesia can exacerbate the compressive effects of an existing mediastinal mass, as summarized in Table 12–3. These changes are related to supine positioning, the effect of anesthetic agents on muscle tone, effects of positive pressure ventilation and the effects of the surgical trauma. Several effects of anesthesia lead to reduced lung volume and thoracic cavity size.⁹ These not only increase the relative size of the tumor mass, but also reduce the normal tethering effect that expanded lungs exert on the airways. Inhalational agents have been described to reduce activity of the intercostal muscles, leading to mechanical instability and inward movement of the rib cage during inspiration.¹⁰ These effects of inhalational agents can linger after extubation in the early postoperative period. While most general anesthetic agents decrease tone of the intercostal muscles and diaphragm, muscle relaxants will obviously exacerbate this. Additionally, muscle paralysis and positive pressure ventilation abolish the negative intrapleural pressure that dilates and opens the airways during inspiration.

Table 12–3. Physiological Changes During Anesthesia and Surgery

Positive pressure ventilation also increases the velocity of gas flow, which in the presence of critical airway stenosis, will result in disruption of laminar flow and creation of turbulence, significantly increasing the resistance to airflow.¹¹ Induction of general anesthesia is not the only dangerous period, however. Severe respiratory compromise has been described during emergence and extubation as well.^1,12

Changes in position and reduced negative intrathoracic pressure might also exacerbate the effects of SVC syndrome, cardiac tamponade or pulmonary artery compression, leading to sudden hypotension, hypoxemia or even cardiac arrest during induction of general anesthesia or positional changes. Both spontaneous breathing and positive pressure ventilation in the setting of partial airway obstruction can lead to dynamic hyperinflation and auto-PEEP, resulting in a decrease in venous return to the heart and exacerbation of preexisting vascular compression.

Only a few case reports of pulmonary artery obstruction from a mediastinal mass exist, probably because the main pulmonary artery and its bifurcation are relatively shielded by the bigger and high-pressure ascending aorta. However, the right ventricular outflow tract might be more susceptible because of its superficial location in the heart and low-pressure status. Indeed, an experimental study of mediastinal masses in dogs has shown significant right ventricular outflow obstruction resulting in right ventricular dilatation, leftward shift of the interventricular septum and a decrease in left ventricular size and stroke volume, leading to decreased cardiac output.¹³ At baseline, the right heart can usually compensate for increased afterload caused by either pulmonary artery or outflow tract compression. However, any further decrease in preload (hypovolemia, increased intrathoracic pressure, anesthetic agents) or in contractility (anesthetic agents) might override the compensatory mechanisms, leading to hypotension, cyanosis and cardiovascular collapse.

Preoperative Evaluation

SIGNS AND SYMPTOMS

While asymptomatic patients are certainly not immune from developing severe cardiorespiratory compromise during anesthesia, patients with symptoms at baseline usually have the most significant reduction in airway and/or blood vessel diameter. In a large pediatric case series, 60% of the patients presented with respiratory findings, and 43% of these (13 out of 30) had significant tracheobronchial compression on computerized tomography (CT) scan, while none of 20 asymptomatic children had tracheobronchial compromise.⁸ In another series of 48 children, all 7 patients who developed complications during anesthesia had at least three respiratory signs and symptoms (cough, shortness of breath, orthopnea, pleural effusion, use of accessory muscles, stridor or a history of respiratory arrest), while only 17% of patients without complications had three or more symptoms.³

SPIROMETRY

The importance of upright and supine spirometry to evaluate the severity of airway obstruction before surgery was initially suggested by Neuman et al in 1984.¹² Classically, reduced airflow in the inspiratory limb of the flow-volume curve is considered a sign of extra-thoracic obstruction, while reduced flow in the expiratory limb, specifically mid-expiratory flow plateau, signifies an intrathoracic obstruction. In a fixed obstruction, where the airway wall is immobile, flow is reduced in both inspiration and expiration regardless of the location of the obstruction (Figure 12–2).¹⁴ In normal healthy adults, a change from sitting to a supine position is accompanied by only a mild decline in spirometric values.¹⁶ Decreases of more than 10% in airflow indices when changing from sitting to supine, or around 20% upon change from standing to supine, are usually considered indicative of pathology.¹⁷ A disproportional reduction of maximal expiratory flow can be a sign of tracheomalacia, which entails a risk of dynamic airway collapse especially after tracheal extubation. It should be stressed that simple spirometric indices such as forced expiratory volume in 1 second (FEV₁) do not change until airway obstruction is very advanced, and therefore flow-volume loops are recommended in these cases.¹⁵

Figure 12–2. Flow-volume loops from a spirometry study of a normal subject, a patient with a fixed upper airway obstruction (UAO) and a patient with COPD. Note the reduction in both inspiratory and expiratory flows and the mid-expiratory flow plateau in the patient with upper airway obstruction. (Reproduced with permission from the American College of Chest Physicians. Diagnosis of upper airway obstruction by pulmonary function testing. Chest. 1975;68(6):796-799.)

Recent data, however, call into question the utility of spirometry for predicting complications in patients with mediastinal masses. Hnatiuk et al have studied 37 adults with various types of mediastinal masses, all of who had undergone preoperative spirometry, and 10 of which had both supine and either upright or sitting studies. Four patients had abnormal spirometry and all had undergone surgery under general anesthesia without complications. Of the five patients with tracheobronchial compression on CT, only one had a positive spirometry test.¹⁷

In another study, flow-volume loops were constructed for 25 patients with intrathoracic Hodgkin lymphoma, 9 of them with radiologic evidence of moderate to severe tracheal compression. Despite this, none of the patients demonstrated variable expiratory flow pattern, and 7 of them had an inspiratory plateau typical of extrathoracic obstruction.¹⁵ Of patients with both inspiratory and expiratory flow limitation, the same number of patients had only mild tracheal compression on CT as the number who had severe compression. The authors speculated that the classical descriptions of the effects of airway obstruction on flow-volume loops might be applicable to intraluminal obstruction, but less so for extrinsic compression of the airways typical of mediastinal masses.

Simpler to measure than flow-volume loops, peak expiratory flow rate (PEFR) has been used to evaluate patients with suspected airway obstruction. In one study on adults, PEFR less than 40% of the predicted value was associated with a 10-fold increase in the risk for postoperative respiratory complications, though no intraoperative respiratory events occurred in this group.⁵ PEFR measurement requires the subject’s cooperation, and therefore may not be useful in young children. More studies are required to define its place in evaluating older children and adults with a mediastinal mass.

RADIOGRAPHIC EVALUATION

A plain chest x-ray will usually show the mediastinal tumor, and may provide the clinician with a rough estimation of its size. In a study of 97 patients with Hodgkin disease, a postero–anterior chest x-ray was used to calculate the ratio between the widest diameter of the mediastinal mass and the width of the thorax at T5-6 (termed mediastinal thoracic ratio, MTR). An MTR greater than 0.5 was associated with a higher incidence of postoperative respiratory complications.¹⁸

However, a plain chest radiograph is not sufficient to assess the involvement of the tracheobronchial tree accurately; therefore a CT scan is always necessary (Figure 12–3).⁸ The value of CT in the prediction of intraoperative complications has been demonstrated repeatedly. In one pediatric series, all 37 patients without tracheobronchial or cardiac compromise on CT scan underwent general anesthesia with no complications, while severe airway obstruction developed in 5 of 8 patients with tracheobronchial compression who underwent general anesthesia. In this series, tracheal narrowing greater than 50% in cross-sectional area was associated with an increased risk of airway obstruction during anesthesia.⁸ In another series of 48 children undergoing general anesthesia, radiologic evidence of tracheal or bronchial compression was found in all 7 patients with intraoperative complications but in only 7 of 41 patients without complications.³ However, a more recent study described a series of 46 children with mediastinal mass, 18 with radiological evidence of tracheal compression or deviation and 24 with evidence of cardiac compromise. All of them underwent general anesthesia, about half using spontaneous ventilation. Only three patients developed respiratory complications, all benign and probably unrelated to the mediastinal mass.¹⁹

Figure 12–3. Thoracic CT scan of a 29-year-old woman with non-Hodgkin lymphoma. Arrow A points to a dilated azygos vein from SVC syndrome while arrow B points to a greater than 50% compression of the trachea just above the carina. (Reproduced with permission from Szokol JW, Alspach D, Mehta MK, Parilla BV, Liptay MJ. Intermittent airway obstruction and superior vena cava syndrome in a patient with an undiagnosed mediastinal mass after cesarean delivery. Anesth Analg. 2003;97(3):883-884.)

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