Thoracic Anesthesia

PART 2

Thoracic Anesthesia Practice


CHAPTERS


 

12
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

image

Figure 12–1. Subdivisions of the mediastinum. (Modified with permission from Benumof JL. Anesthesia for Thoracic Surgery. 2nd ed. Philadelphia: WB Saunders;1995:39. Copyright © Elsevier.)

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

image

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

image

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

image

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

image

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

image

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.)

In a case series of 105 adults with mediastinal mass, 8 patients had tracheal compression of more than 50% cross-sectional area and 4 patients had compression of the main stem bronchus. There were no intraoperative airway problems in this series. However, tracheal compression was a risk factor for postoperative respiratory complications such as pneumonia and atelectasis. In addition, pericardial effusion on CT was a risk factor for intraoperative cardiovascular complications.5

MRI studies are at least as useful as CT imaging, and may offer some advantages in several specific tumor types. Both studies are done in a supine position, similar to anesthesia and surgery, and can therefore demonstrate positional compression effects of the tumor mass. It is important that the imaging studies be performed as near as possible to the time of surgery, as the tumor may grow rapidly.6

FLEXIBLE FIBEROPTIC BRONCHOSCOPY

While usually impractical in small children, this study can be very useful in older children and adults. Not only can it be used to explore airway anatomy and show areas and degree of obstruction, but it can help assess the effect of change in position on the degree of obstruction (Figure 12–4).20 It can also be used for awake intubation during spontaneous breathing or in the patient with suspected difficult visualization of the airway, or who does not tolerate the supine position without respiratory compromise.2 Fiberoptic bronchoscopy can also be used to guide the endotracheal tube beyond the point of obstruction.

image

Figure 12–4. Flexible bronchoscopy views in a 24-year-old patient with Hodgkin lymphoma in supine position (A) and sitting (B). (Reproduced with permission from Prakash UB, Abel MD, Hubmayr RD. Mediastinal mass and tracheal obstruction during general anesthesia. Mayo Clin Proc. 1988;63(10):1004-1011.)

ECHOCARDIOGRAPHY

Echocardiography can delineate tumor involvement of the heart and great vessels. It can accurately assess the degree of pulmonary artery or right ventricular outflow tract encroachment, the existence of pericardial effusion and the presence of cardiac tamponade, and the degree of ventricular dysfunction related to myocardial infiltration. Some preoperative signs and symptoms that would be an indication for a preoperative echocardiography study include orthopnea, cyanosis, jugular venous distension, pulsus paradoxus and syncope.5 Rarely, transesophageal echocardiography may show the tumor itself when it surrounds the heart.21

Incidence and Prediction of Perioperative Complications

Many anecdotal case reports have been published describing perioperative complications in patients with mediastinal masses.12,20-26 While these are instructive, they do not give much information about the prevalence of these complications. However, several case series have been published and are summarized in Table 12–4. Most of the existing data is on children. Importantly, it seems that the incidence of intraoperative respiratory complications, especially airway obstruction, is much smaller in adults, as might be predicted by the anatomical differences.5,27 A search of various closed claims databases performed in 2001 found eight cases related to anterior mediastinal masses, five of them occurring in children less than 8-years old and only one case in an adult above 18 years of age.6

Table 12–4. Incidence of Intraoperative Complications in Patients with Mediastinal Masses

image

While intraoperative complications are the major source of concern for the anesthesiologist, postoperative respiratory complications have been described too and, in adults, might be more significant. These include airway edema, atelectasis and pneumonia, and usually occur within the first 48 hours.5

Our ability to predict which patient with a mediastinal mass will develop complications with general anesthesia is still limited. Various authors have suggested different predictors; however, most of these studies have been performed in children and their relevance for the adult population is questionable. Also, the number of subjects, and especially the number of those who developed complications, is relatively small, limiting the power of statistical multivariate analysis. The most rigorous analysis was performed by Ng et al and is summarized in Table 12–5. Important risk factors that were consistently found in various studies include an anterior (vs middle or posterior) mediastinal mass, preoperative presence of significant respiratory signs and symptoms, radiologic evidence of significant (above 35%-50%) narrowing of the tracheal cross-sectional area and the presence of SVC syndrome. In one large series in adults, only pericardial effusion was found to be a risk factor for intraoperative complications (which were mostly cardiovascular), while the presence of severe orthopnea, stridor, cyanosis or jugular vein distension, tracheal narrowing of more than 50%, PEFR less than 40% predicted, and a mixed restrictive-obstructive picture on spirometry were all predictors of postoperative respiratory complications.5

Table 12–5. Predictors of Complications during General Anesthesia in Children with a Mediastinal Mass

image

ANESTHETIC MANAGEMENT

The governing principle when anesthetizing a patient with a mediastinal mass is “Noli Pontes Ignii Consumere” (don’t burn your bridges). Basically, the anesthesiologist should plan his interventions striving to keep available as many viable alternatives as possible should a catastrophic cardiorespiratory complication occur.

Procedures such as CT-guided needle biopsy, cervical lymph node biopsy, or diagnostic thoracentesis to obtain a tissue diagnosis should be done under local anesthesia, if at all possible. The use of EMLA cream and ketamine sedation can facilitate these procedures in young children.

If general anesthesia is essential, consideration should be given to preoperative irradiation and/or chemotherapy in an attempt to reduce the size of a large obstructing tumor, for example Hodgkin lymphoma or neuroblastoma, thereby decreasing preoperative symptoms and respiratory compromise.8,18 In a large series of patients with Hodgkin disease who presented for surgery with a mediastinal mass, all five respiratory complications occurred in the 74 patients who did not receive preoperative radiation therapy, while none of 24 patients who did receive radiation therapy had any respiratory complication.1 It should be taken into account, however, that such preoperative therapy might distort the histopathological appearance of the tumor and hinder accurate diagnosis. For patients with large, symptomatic pericardial effusions, preoperative drainage under local anesthesia can decrease the risk of intraoperative hypotension.

Once the decision is made to proceed with general anesthesia, a detailed plan should be formulated and discussed ahead of time with the other members of the surgical team. (Table 12–6).

Table 12–6. Principles of Anesthesia for the Patient with a Mediastinal Mass

image

Induction of Anesthesia

An important concept when inducing anesthesia is the preservation of spontaneous breathing whenever possible. This usually requires either a deeper level of anesthesia for airway manipulation (more so for endotracheal intubation than for a laryngeal mask airway)28 or an awake fiberoptic intubation if difficult intubation is expected or if it is thought that the patient will not be able to tolerate the hemodynamic consequences of deep anesthesia. Topical airway anesthesia or the use of airway nerve blocks will also allow maintaining a lighter plane of anesthesia, reducing muscular hypotonicity and facilitating rapid awakening if deemed necessary. Typically, inhalational induction is chosen to preserve spontaneous breathing. If propofol is chosen for induction, slow infusion rather than a bolus dose should be used. Another choice for an IV induction agent is ketamine, which usually preserves spontaneous breathing and minimizes hemodynamic depression due to its sympathomimetic properties.29Some have suggested the use of PEEP of 10 to 15 cm H2O in addition to spontaneous ventilation, to “stent” the airways open.8

Avoiding sedation in the premedication is advocated due to the risk of airway obstruction. In one closed claim case, an adult with a mediastinal mass developed cardiac arrest after sedation and before induction of anesthesia.6 Antisialagogues can be helpful if awake fiberoptic intubation is contemplated.

If muscle paralysis is deemed necessary for the surgical procedure, the patient should be induced and the airway controlled while still spontaneously breathing. Then assisted breaths can be gradually added using a bag and mask, so the effect of positive pressure breaths on airway patency and hemodynamics can be evaluated before committing to a muscle relaxant, preferably a short-acting one.

Once the chest is opened, muscle paralysis can be safely employed and the patient placed on mechanical ventilation. The surgeon might be asked to mechanically lift the tumor mass to relieve airway compression.30

Optimal body positioning should be determined for symptomatic patients. Many will be more symptomatic in a supine position, and sitting them up by elevating the back of the operating table might alleviate the obstruction. For some tumors, positioning the patient in the lateral position might relieve pressure on the carina, especially with off-center masses. In the rare patient, severe intraoperative airway obstruction or cardiovascular collapse might only be relieved by sitting, leaning forward, or even prone positioning. Some have recommended the routine use of a semi-recumbent position for induction of general anesthesia in these patients. The danger of a massive venous air embolism in the sitting position for a thoracic or neck operation, however, is real.

Airway Management

Several options exist for instrumentation of the airway. As mentioned before, a laryngeal mask can be inserted under a relatively lighter level of anesthesia, and is an ideal solution for a spontaneously breathing patient. However, it does not allow rapid bypass of a developing complete obstruction. Also, spontaneous breathing is usually not advocated during thoracotomy, although it is not impossible.11

In addition to a regular endotracheal tube, several other options exist that allow passing a breathing tube beyond the point of obstruction, either preemptively or once an obstruction does develop and is not rapidly relieved by a change in patient position. This can be achieved in children by using an armored endotracheal tube passed intra-bronchially if needed30 and in adults by either an armored endotracheal tube or by a double lumen tube. Another option is to advance two small diameter long tubes (called microlaryngeal tubes) one into each main bronchus under direct fiber-optic visualization.23

Management of Complications

Typically, initial signs of airway obstruction such as wheezing and reduced breath sounds are mistaken to be evidence of bronchospasm or tension pneumothorax, and precious time is lost. In a patient with suggestive anatomy, the possibility of major airway obstruction should be entertained early and adequate treatment delivered promptly.6

If airway obstruction develops, a change in patient position may relieve it. Passing a tube beyond the point of obstruction, as described above, is another option. A rigid bronchoscope, and a surgeon experienced in its use, should always be available in high-risk patients, as the obstruction may hinder passage of a soft tube. The use of a helium-oxygen mixture has been suggested to decrease turbulence and resistance to airflow in an obstructed airway.31

If hypotension develops, the experimental studies described earlier suggest that right ventricular (RV) outflow obstruction leading to RV failure is the most commonly responsible mechanism.13Vasopressor therapy aimed at improving coronary perfusion is the treatment of choice. However, an element of reduced preload, especially in patients with known SVC compression, might coexist, and a judicious fluid bolus should be given as well. Over-hydration, however, is counterproductive in patients with RV failure, as it will only lead to increased RV distension, more leftward displacement of the interventricular septum, and decreased left ventricular loading. It has been described that cyanosis due to pulmonary artery compression can be reversed by either resumption of spontaneous breathing32,33 or by a change to the sitting position.22

If all else fails, and respiratory or hemodynamic deterioration continues, two options still exist—either rapidly awakening the patient, if possible, or emergency surgical intervention—median sternotomy with mechanical elevation of the tumor off the airways and blood vessels,21,33 or emergency cardiopulmonary bypass (CPB).

Cardiopulmonary Bypass—Elective or on Standby?

Several reports exist in the literature where standby CPB was available in patients with a mediastinal mass; however in only a few was CPB eventually required and used.26 It is questionable whether cannulation for CPB could be performed fast enough in a patient who develops severe cardiorespiratory compromise on the verge of arrest, and especially when the patient is not supine, eg, in a lateral position for thoracic surgery.34 Therefore, some authors have chosen to electively cannulate the femoral vessels under local anesthesia before induction of general anesthesia, or even to commence CPB with induction of general anesthesia, instead of having CPB on stand-by status only.32,35,36 It is highly unlikely that a study could ever be conducted to decide which approach is better. The decision should therefore be individualized, based on both the patient’s risk (eg, a patient with a large mass that compresses the pulmonary artery and trachea, or with severe SVC syndrome is at a higher risk for complications around induction of anesthesia) and the preference of the surgical team (highly experienced surgeon and perfusionist could accomplish emergency cannulation and CPB faster). If the standby CPB approach is chosen, the CPB machine should be primed, the cannulation lines ready, the groins prepared and sterilely draped, and both perfusionist and cardiac surgeon available in the operating room before induction of anesthesia.

Suggested Perioperative Approach

Several algorithms have been suggested to guide the surgeon and anesthesiologist in managing patients with mediastinal masses; one is presented in Figure 12–5. Generally, in the presence of clinical or radiological evidence of severe tracheobronchial obstruction, general anesthesia should be reserved for selected patients who have the prospect of a curative procedure. In this case, all the above precautions should be taken and the use of CPB should be considered. Otherwise, an attempt to achieve tissue diagnosis by biopsy under local anesthesia, or preoperative tumor shrinkage with chemotherapy or radiotherapy, is recommended. In the patient with no radiological evidence of tracheobronchial obstruction, proceeding to surgery under general anesthesia can be done relatively safely. The utility of a similar algorithm was tested in a series of 31 children with anterior mediastinal mass. Surgery under local anesthesia was chosen if either tracheal cross-sectional area or PEFR were less than 50% of predicted values, otherwise general anesthesia was used. No complications have occurred with this management policy,37 though patient number was too small to provide a definitive proof of safety.

image

Figure 12–5. Suggested algorithm for management of patients with anterior mediastinal mass. (Reproduced with permission from Azizkhan RG, Dudgeon DL, Buck JR, et al. Life-threatening airway obstruction as a complication to the management of mediastinal masses in children. J Ped Surg. 1985;20(6):816-822. Copyright © Elsevier.)

SUPERIOR VENA CAVA SYNDROME

The SVC syndrome results from compression of the SVC, leading to obstructed venous return from the upper half of the body. It is most commonly caused by an extrinsic compression from a mediastinal tumor, mainly bronchogenic carcinoma or lymphoma, though it has been reported to occur due to intravascular caval thrombosis.38 The clinical manifestations depend to a large extent on the rapidity of development of the obstruction, as slow development will allow collateral veins to develop and decompress the engorged venous system. The severity of the signs and symptoms also depends on the location of the obstruction to blood flow relative to the entry point of the azygos vein into the SVC—obstruction above the insertion of the azygos vein will allow drainage of blood from the upper body through short collaterals to the azygos vein, resulting in milder symptoms. A rapidly developing SVC syndrome will result in edema and either plethora or cyanosis of the face, neck, and upper extremities, conjunctival edema, hemoptysis, dyspnea (especially on exertion), and sometimes symptoms and signs of increased intracranial pressure like headache, blurred vision, and papilledema. The distended veins in the upper torso will typically not collapse when the patient assumes the sitting position. In addition to visible edema, some patients might develop tracheobronchial and upper airway mucosal edema causing respiratory symptoms (dyspnea, cough, nasal stuffiness) or difficult airway visualization during intubation. The signs and symptoms of SVC syndrome will typically worsen while supine or leaning forward.

Evaluation of the patient with suspected SVC syndrome requires CT or a magnetic resonance imaging study to define any existing tumor, as well as an echocardiographic study to evaluate the extent of caval obstruction and any coexisting cardiac pathology (eg, pericardial effusion).39

Treatment of SVC syndrome is frequently palliative only, as the underlying malignant disease is usually widespread. Supportive measures include elevation of the head, oxygen, and diuretics. Steroids, chemotherapy, or radiotherapy may be used to reduce tumor size and symptoms as well as to decrease the risk of induction of general anesthesia (see below). Operative options include intravascular stenting, tumor debulking, thrombectomy, and vena cava bypass.6

Anesthetic Management

While patients might be only mildly symptomatic at baseline, induction of general anesthesia can lead to cardiovascular collapse. This is caused by a further reduction in cardiac preload, related to the vasodilatory effects of anesthetic agents, increased compression by the tumor mass, and the effect of positive pressure ventilation. Preoperative radiation or chemotherapy might be especially beneficial in alleviating SVC obstruction, if possible. Otherwise, it is very important to treat any preexisting hypovolemia before induction of anesthesia. The use of anesthetic agents with less vasodilatory and negative inotropic effects, (such as etomidate and ketamine), is preferable. Because venous return from the upper half of the body might be limited or even interrupted, it is important to secure intravenous access in the lower extremities. Bleeding might be excessive due to increased central venous pressure, so adequate venous access and cross-matched blood should be available. Central venous and pulmonary artery catheters, if planned, should also be placed through a femoral vein. All patients should be carefully evaluated for the existence of airway edema. In selected cases, awake fiberoptic intubation might be preferable over regular laryngoscopy.40 Last, it is very important to maintain systemic blood pressure around baseline values in order to avoid a reduction in cerebral perfusion pressure, as resistance to venous outflow from the head and brain is elevated. Special neuromonitoring modalities, (cerebral oximetry, transcranial Doppler), might help to provide early clues of cerebral hypoperfusion.41 Table 12–7summarizes recommendations for anesthetizing patients with SVC syndrome.

Table 12–7. Anesthetic Considerations for the Patient with Superior Vena Cava Syndrome

image

REFERENCES

1. Piro AJ, Weiss DR, Hellman S. Mediastinal Hodgkin’s disease: a possible danger for intubation anesthesia. Intubation danger in Hodgkin’s disease. Int J Rad Oncol Biol Phys. 1976;1(5-6):415-419.

2. Pullerits J, Holzman R. Anaesthesia for patients with mediastinal masses. Can J Anesth. 1989;36(6):681-688.

3. Ng A, Bennett J, Bromley P, Davies P, Morland B. Anaesthetic outcome and predictive risk factors in children with mediastinal tumours. Pediatr Blood Cancer. 2007;48(2):160-164.

4. Lerman J. Anterior mediastinal masses in children. Sem Anesth Periop Med Pain. 2007;26:133-140.

5. Béchard P, Létourneau L, Lacasse Y, Côté D, Bussières JS. Perioperative cardiorespiratory complications in adults with mediastinal mass. Anesthesiology. 2004;100(4):826-834.

6. Narang S, Harte BH, Body SC. Anesthesia for patients with a mediastinal mass. Anesthesiol Clin North Am. 2001;19(3):559-579.

7. Crosby E. Clinical case discussion: anesthesia for Cesarean section in a parturient with a large intrathoracic tumour. Can J Anaesth. 2001;48(6):575-583.

8. Azizkhan RG, Dudgeon DL, Buck JR, et al. Life-threatening airway obstruction as a complication to the management of mediastinal masses in children. J Pediatr Surg. 1985;20(6):816-822.

9. Bergman NA. Reduction in resting end-expiratory position of the respiratory system with induction of anesthesia and neuromuscular paralysis. Anesthesiology. 1982;57(1):14-17.

10. Jones JG, Faithfull D, Jordan C, Minty B. Rib cage movement during halothane anaesthesia in man. Br J Anaesth. 1979;51(5):399-407.

11. Sibert KS, Biondi JW, Hirsch NP. Spontaneous respiration during thoracotomy in a patient with a mediastinal mass. Anesth Analg. 1987;66(9):904-907.

12. Neuman GG, Weingarten AE, Abramowitz RM, Kushins LG, Abramson AL, Ladner W. The anesthetic management of the patient with an anterior mediastinal mass. Anesthesiology. 1984;60(2):144-147.

13. Johnson D, Hurst T, Cujec B, Mayers I. Cardiopulmonary effects of an anterior mediastinal mass in dogs anesthetized with halothane. Anesthesiology. 1991;74(4):725-736.

14. Brookes GB, Fairfax AJ. Chronic upper airway obstruction: value of the flow volume loop examination in assessment and management. J R Soc Med. 1982;75(6):425.

15. Vander Els NJ, Sorhage F, Bach AM, Straus DJ, White DA. Abnormal flow volume loops in patients with intrathoracic Hodgkin’s disease. Chest. 2000;117(5):1256-1261.

16. Vilke GM, Chan TC, Neuman T, Clausen JL. Spirometry in normal subjects in sitting, prone, and supine positions. Respir Care. 2000;45(4):407-410.

17. Hnatiuk OW. Spirometry in surgery for anterior mediastinal masses. Chest. 2001;120(4):1152-1156.

18. Turoff RD, Gomez GA, Berjian R, et al. Postoperative respiratory complications in patients with Hodgkin’s disease: relationship to the size of the mediastinal tumor. Eur J Cancer Clin Oncol. 1985;21(9):1043-1046.

19. Stricker P, Gurnaney H, Litman R. Anesthetic management of children with an anterior mediastinal mass. Anesthesiology. 2006;105:A970.

20. Prakash UB, Abel MD, Hubmayr RD. Mediastinal mass and tracheal obstruction during general anesthesia. Mayo Clin Proc. 1988;63(10):1004-1011.

21. Lin C-M, Hsu J-C. Anterior mediastinal tumour identified by intraoperative transesophageal echocardiography. Can J Anesth. 2001;48(1):78-80.

22. Alkhafaji S, Mazhar R, Carr CS, Alkhulaifi AM. Extreme cardiac and pulmonary artery compression causing positional oxygen desaturation. Emerg Med J. 2008;25(8):541.

23. John RE, Narang VP. A boy with an anterior mediastinal mass. Anaesthesia. 1988;43(10):864-866.

24. Keon TP. Death on induction of anesthesia for cervical node biopsy. Anesthesiology. 1981;55(4):471-472.

25. 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.

26. Takeda S-i, Miyoshi S, Omori K-i, Okumura M, Matsuda H. Surgical rescue for life-threatening hypoxemia caused by a mediastinal tumor. Ann Thorac Surg. 1999;68(6):2324-2326.

27. Azarow KS, Pearl RH, Zurcher R, Edwards FH, Cohen AJ. Primary mediastinal masses. A comparison of adult and pediatric populations. J Thorac Cardiovasc Surg. 1993;106(1):67-72.

28. Hattamer SJ, Dodds TM. Use of the laryngeal mask airway in managing a patient with a large anterior mediastinal mass: a case report. AANA J. 1996;64(5):497-500.

29. Frawley G, Low J, Brown TC. Anaesthesia for an anterior mediastinal mass with ketamine and midazolam infusion. Anaesth Intensive Care. 1995;23(5):610-612.

30. Vas L, Falguni N, Veena N. Anaesthetic management of an infant with anterior mediastinal mass. Paediatr Anaesth. 1999;9(5):439-443.

31. Polaner DM. The use of heliox and the laryngeal mask airway in a child with an anterior mediastinal mass. Anesth Analg. 1996;82(1):208-210.

32. Hall KD, Friedman M. Extracorporeal oxygenation for induction of anesthesia in a patient with an intrathoracic tumor. Anesthesiology. 1975;42(4):493-495.

33. Levin H, Bursztein S, Heifetz M. Cardiac arrest in a child with an anterior mediastinal mass. Anesth Analg. 1985;64(11):1129-1130.

34. Slinger P, Karsli C. Management of the patient with a large anterior mediastinal mass: recurring myths. Curr Opin Anaesth. 2007;20(1):1-3.

35. Inoue M, Minami M, Shiono H, et al. Efficient clinical application of percutaneous cardiopulmonary support for perioperative management of a huge anterior mediastinal tumor. J Thorac Cardiovasc Surg. 2006;131(3):755-756.

36. Tempe DK, Arya R, Dubey S, et al. Mediastinal mass resection: femorofemoral cardiopulmonary bypass before induction of anesthesia in the management of airway obstruction. J Cardiothorac Vasc Anesth. 2001;15(2):233-236.

37. Shamberger RC, Holzman RS, Griscom NT, Tarbell NJ, Weinstein HJ, Wohl ME. Prospective evaluation by computed tomography and pulmonary function tests of children with mediastinal masses.Surgery. 1995;118(3):468-471.

38. Barbeito A, Bar-Yosef S, Lowe JE, Atkins BZ, Mark JB. Unusual cause of superior vena cava syndrome diagnosed with transesophageal echocardiography. Can J Anaesth. 2008;55(11):774-778.

39. Ayala K, Chandrasekaran K, Karalis D, Parris T, Ross J. Diagnosis of superior vena caval obstruction by transesophageal echocardiography. Chest. 1992;101(3):874-876.

40. Shapiro HM, Sanford TJ, Schaldach AL. Fiberoptic stylet laryngoscope and sitting position for tracheal intubation in acute superior vena caval syndrome. Anesth Analg. 1984;63(2):161-162.

41. Reece IJ, al Tareif H. Surgical interruption of the superior vena cava. J Thorac Cardiovasc Surg. 1995;109(5):1020.