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Mediastinal Mass

Contributing Author: Danielle Van Damme MSN, CPNP-AC, University of Michigan Pediatric Critical Care

Etiology and Epidemiology

35-55% occur in the anterior mediastinum 
30-40% occur in the posterior mediastinum
15% occur in the middle mediastinum
Tumors arise from many tissue types:

o Lymphatic (most common in pediatrics)
o Thymus
o Neurogenic
o Germ cell neoplasm
o Bronchogenic
o Metastatic

Figure 1: The Medisastinum 

Figure 2: Possible Etiology Based on Mediastinal Location (BMJ Best Practices)

Clinical Presentation

Initial signs
o Typically present with respiratory findings. 
o Symptoms may be acute or gradual, depending on the rate of growth of the tumor and involved structures
o Severity of symptoms are not always predictive of degree of compromise
o Often mediastinal masses are incidental findings on chest radiograph. 

o Orthopnea
o Dyspnea
o Cough
o Wheezing- Not all that wheezes is asthma! Hence, one of the reasons first time wheezers should have a CXR done
o Pleural effusion
o Stridor
o Hoarseness

o Tachycardia
o Jugular vein distension
o Swollen face
o Syncope
o Cyanosis 
o Pericardial effusions (tamponade physiology)

o Fever
o Night sweats
o Weight loss
o Pain (pleuritic, chest, neck, back)


o Compression of pulmonary arteries leads to decreased pulmonary perfusion
o Pulmonary edema occurs from pulmonary vein compression and vascular congestion
o Compression of trachea or bronchus

Figure 3. Airway Compression of Left Main Bronchus (LMB) by anterior mediastinal mass (MM). PE= pleural effusion. (Harte et al, Anesthesiology 2002)

o Compression of airways can lead to air trapping and elevated carbon dioxide

Hemodynamic instability
o Compression of the right heart chambers, superior vena cava, pulmonary arteries
o Leads to decreased left ventricular preload and cardiac output
o Right heart failure from increased pulmonary artery resistance 
o Pericardial effusions leading to tamponade 

Superior Vena Cava Syndrome
o Compression of the superior vena cava leads to dilation of the surrounding vessels and collaterals
o Increased vascular resistance leads to edema of surrounding superior tissues


o Chest radiograph 
o Computed Tomography of the chest to measure the degree of compression of trachea, bronchi, and vasculature if this can be done safely without sedation
o MRI may be useful as a secondary diagnostic tool, as it can provide better differentiation between structures, however it will require more time and limited movement.  
o Echocardiogram to assess cardiac output, pulmonary blood flow, and tamponade physiology
o Pulmonary Function Test
o Biopsy of the thoracic or extrathoracic tissue.  Thoracic nodes are likely the primary mass, but impose risk of cardiopulmonary compromise.  Extrathoracic biopsies have demonstrated to be an effective diagnostic strategy while limiting the complications (Acker et al, 2015). Again, biopsies should be very carefully planned given the significant risks of loss of muscle tone and further airway or vascular collapse with sedation that may not be alleviated via endotracheal intubation (ie ETT doesn't reach past point of obstruction) and rapidly lead to death. Critical care, anesthesiology, oncology, surgery, and ECMO teams should all be in discussion regarding this high risk procedure. 

o Positioning of the patient may be essential (left lateral decubitus or prone) to temporarily alleviate the effects of extrinsic compression
o Maintaining spontaneous ventilation will typically maintain adequate negative intrathoracic pressure to prevent the effect of gravity on the intrathoracic structures.
o If endotracheal intubation required, consider awake fiberoptic intubation to avoid sedatives. This should be well planned and discussed with anesthesia, surgery, and ECMO as a backup option. 

o Multiple disciplinary approach with Pediatric surgeon, Pediatric oncologist, Pediatric intensivist, anesthesiology, and ECMO backup when airway or vascular compression is suspected. Ie if patient is wheezing or has respiratory distress with concern for a mediastinal mass, extreme caution is vital. 
o Depending on the patient stability and risk of cardiopulmonary compromise, may start empiric high-dose steroids, radiation, or chemotherapy
o Avoid sedative and neuromuscular blockade agents
o ECMO on standby for high risk cardiopulmonary collapse

Figure 4.  Example algorithm used in a study by Perger, Lee, and Shamberger (2008) of 40 patients with anterior mediastinal mass and critical airway. 

Specific Anesthesia Concerns

Anterior mediastinal masses are at particular risk for cardiopulmonary collapse when sedated.
Anesthesia magnifies the effect of the mass with smooth muscle relaxation and more collapsible airways and vasculature.
Blocking of spontaneous respiration causes increase in intrathoracic pressure
Spontaneous inspiration maintains negative pressure and patency of airway, which will prevent complete obstructive effect of the mass.

Supine position 
o Increases compression with the effect of gravity and worsens V/Q mismatch
o Diaphragm moves cephalad which increases intrathoracic pressure

Positive Pressure Ventilation
o Endotracheal intubation may not reach past the point of obstruction which can just worsen the obstruction with an endotracheal tube.
o      Positive pressure ventilation can increase intrathoracic pressure which may worsen compression of vascular structures


1) Aker, S.N., Linton, J., Tan, G.M., Garrington, T.P., Bruny, J., Hilden, J.M., Hoffman, L.M., and Partrick, D.A. (2015). A multidisciplinary approach to the management of anterior mediastinal masses in children. Journal of Pediatric Surgery, 50, 875-878.

2) Lerman, J. (2007). Anterior mediastinal masses in children. Seminars in Anesthesia, Perioperative Medicine and Pain, 26, 133-140. 

3) Nichols, D.G. (2008). Roger’s Textbook of Pediatric Intensive Care (4th Ed). Philadelphia, PA: Lippencott Williams & Wilkins.

4) Perger, L, Lee, E., Shamberger, R. (2008). Management of children and adolescents with a critical airway due to compression by an anterior mass.  Journal of Pediatric Surgery, 43(11), 1990-1997.