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Thoracic Emergencies 

Thoracic Emergencies
Thoracic Emergencies

Peter S. Burrage

, Marc S. Azran

, and Michael Nurok

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date: 13 June 2021

Bronchopleural Fistula


A communication between the bronchial tree and pleural space that causes a pneumothorax. A bronchopleural fistula (BPF) can be associated with pulmonary resection as well as with chronic infection such as tuberculosis or empyema. After resection, BPF can occur immediately postoperatively (“stump blow out”) or in a more delayed fashion, typically presenting 1–2 weeks later. It may also be caused by penetrating chest trauma or iatrogenic injury such as central line insertion, barotrauma, or volutrauma caused by mechanical ventilation.


  • Inability to ventilate (complete stump blowout)

  • Dyspnea

  • Oxygen desaturation

  • Increased inspiratory pressures

  • Cyanosis

  • Hypotension

  • Tachycardia

Differential Diagnosis

  • Endotracheal tube malposition

  • Bronchospasm

  • Extrinsic lung compression by a mass or fluid

  • Hemothorax

  • Cardiac tamponade

Immediate Management

  • Immediate postoperative stump blowout:

    • Isolate the lungs with a double-lumen endotracheal tube or bronchial blocker (see page [link]).

    • Insert a thoracostomy tube.

    • Schedule the patient for emergency surgical re-exploration.

  • Delayed bronchopleural fistula

    • Insert a thoracostomy.

    • A bronchopleural fistula may permit airflow up to 16 liters/min (LPM) across the defect. A thoracostomy tube with an internal diameter of at least 6 mm is required to evacuate air rapidly enough to avoid tension pneumothorax.

    • High volume thoracostomy tube drainage system ideally capable of evacuating up to 35 LPM with a suction pressure of –20 cm H2O.

Diagnostic Studies

  • Chest radiograph after chest tube insertion on the affected side.

  • A CT scan may demonstrate an air fluid level.

Subsequent Management

  • Treat the underlying lung pathology and wean mechanical ventilation. Positive pressure ventilation creates a gradient between the airways and pleural space. This allows air to pass through the fistula and prevents it from closing. Minimizing the volume of the leak during mechanical ventilation promotes healing.

  • Conventional mechanical ventilation

    • Minimize alveolar distension and airway pressure.

    • Use the lowest allowable minute ventilation (both rate and tidal volume).

    • Decrease inspiratory time by altering the I:E ratio or by increasing inspiratory flow rates.

    • Conduct regular spontaneous breathing trials with a view to the earliest possible ventilator liberation.

    • Use weaning modes to encourage spontaneous ventilation.

    • Use the least amount of positive end-expiratory pressure (PEEP) that is feasible.

    • Decrease the amount of chest tube suction as tolerated.

    • Treat bronchospasm and other airflow obstruction aggressively.

  • Alternative modes of ventilation may decrease mean airway pressures.

    • Occlusion of the chest tubes during inspiration or adding PEEP to the chest tube system may minimize the egress of air through the fistula during ventilation; however, creation of a tension pneumothorax is a risk.

    • Placing the patient into the lateral decubitus position with the BPF in the dependent position theoretically decreases airflow through the fistula.

    • Consider differential lung ventilation through a double-lumen endotracheal tube. The normal lung may be ventilated conventionally, whereas the injured lung may be managed with any of the preceding techniques. Two synchronized ventilators are required.

    • High-frequency jet ventilation may be used to maintain oxygenation, but respiratory acidosis may occur because CO2 elimination is decreased.

Invasive Management

  • Bronchoscopy may be used to localize and seal a proximal small BPF with fibrin, autologous blood, or cautery.

  • A distal BPF that cannot be visualized may be occluded with a balloon.

  • Chest tube or thoracoscopic sclerosis may incite an inflammatory response, thereby sealing a BPF.

  • Surgical pleurodesis or bronchial stapling should be considered in refractory cases.

  • Alert the surgical team if the patient requires 100% O2 because electrocautery may cause a fire.

Risk Factors

  • High-risk pulmonary surgery or lung volume reduction surgery

  • Pulmonary infection

  • Central line placement

  • Excessive tidal volumes (>10 mL/kg) in a patient with lung injury

  • Obstructive lung disease with auto-PEEP


Decrease tidal volumes to 6 mL/kg

  • Permissive hypercapnia

  • Reduce inspiratory pressures.

  • Monitor static respiratory compliance while increasing PEEP. Decrease PEEP if compliance falls.

  • Wean the patient from mechanical ventilation early.

  • Institute measures to avoid nosocomial pneumonia.

  • Suspend mechanical ventilation while inserting a needle into the internal jugular or subclavian veins.

  • Surgical reinforcement of stumps with a flap (e.g., intercostal muscle, omental tissue)

Further Reading

Baumann MH, Sahn SA. Medical management and therapy of bronchopleural fistulas in the mechanically ventilated patient. Chest. 1990; 97(3): 721–728.Find this resource:

Boudaya MS, Smadhi H, Zribi H, et al. Conservative management of postoperative bronchopleural fistulas. J Thorac Cardiovasc Surg. 2013; 146(3): 575–579.Find this resource:

Lois M, Noppen M. Bronchopleural fistulas: an overview of the problem with special focus on endoscopic management. Chest. 2005; 128(6): 3955–3965.Find this resource:

Cardiac Herniation after Pneumonectomy


Herniation of the myocardium into an empty hemithorax through a pericardial defect created during pneumonectomy. Both left- and right-sided cardiac herniation may occur, causing severe hemodynamic instability. Mortality is 50% if recognized and 100% if left untreated.


  • Usually occurs during patient transport. May occur within the first 24 hours after surgery.

  • Hypotension

  • Tachycardia

  • Cardiovascular collapse

  • Dysrhythmias

  • Electrocardiogram (ECG) changes (ST segment or axis changes)

  • Right-sided herniation

    • Jugular venous distension

    • Cyanosis of the face

    • Absence of a left-sided cardiac impulse


  • Right-sided cardiac herniation causes cardiac malposition.

    • Torsion of the cavoatrial junction severely impedes venous return.

    • Torsion of the great vessels or ventricular outflow tract obstructs blood flow.

    • The end result is myocardial ischemia and cardiovascular collapse.

  • Left-sided cardiac herniation involves prolapse of the ventricles through the defect.

    • Cardiac orientation and venous return is preserved.

    • Strangulation of the myocardium and epicardial vessels causes myocardial ischemia.

    • Ventricular outflow tract obstruction also may occur.

Differential Diagnosis

  • Myocardial infarction

  • Hypovolemic shock

  • Contralateral pneumothorax

  • Pulmonary embolus

  • Cardiac tamponade

Immediate Management

  • Clinical scenario can help to differentiate between cardiac herniation (which requires immediate surgical intervention) and hypotension due to hypovolemia or deep anesthesia (which responds to fluid administration and/or vasopressors).

Management of Presumed Cardiac Herniation

  • Alert the surgeon immediately.

  • Reposition the patient with the operative side up.

  • Decrease tidal volume and PEEP.

  • Begin aggressive fluid resuscitation to correct relative preload deficiency.

  • Support the blood pressure as necessary with vasopressors. Severe hypotension may require aggressive treatment with an infusion of phenylephrine (0.5–1 mcg/kg/min) or epinephrine (0.03–0.05 mcg/kg/min).

  • If complete cardiac arrest occurs, CPR may make herniation worse, which underscores the importance of immediate surgical intervention and helps explain the high mortality rate of this complication.

  • Surgical correction with reduction of myocardial prolapse and pericardial patch construction.

Diagnostic Studies

  • This is a clinical diagnosis. Do not delay management for diagnostic studies.

  • Chest radiograph

    • Right-sided herniation

    • Opacification of the right hemithorax from mediastinal shift

    • Abnormal (clockwise) configuration of a pulmonary artery catheter

    • Left-sided herniation may show a rounded opacity in the lower left hemithorax due to ventricular strangulation.

  • Echocardiography (TTE or TEE) may reveal prolapsed myocardium or a malpositioned heart.

Risk Factors

  • Pericardial defect of any size and an empty hemithorax

  • Chest tubes placed to suction or water seal

  • Positive pressure ventilation and PEEP

  • Coughing caused by suctioning or extubation

  • Position changes in the operating room or during transport from the operating room (especially when the operative side is down).


The surgeons should use a pericardial sling or patch close large pericardial defects. Primary closure of the pericardium has been used for smaller defects, although herniation can occur from a ruptured suture line.

Further Reading

Chambers N, Walton S, Pearce A. Cardiac herniation following pneumonectomy—an old complication revisited. Anaesth Int Care. 2005; 33(3): 403–409.Find this resource:

Hartigan PM, Ng JM. Anesthetic strategies for patients undergoing extrapleural pneumonectomy. Thorac Surg Clin. 2004; 14(4): 575–583, xi.Find this resource:

Slinger P. Update on anesthetic management for pneumonectomy. Curr Opin Anaesthesiol. 2009; 22(1): 31–37.Find this resource:

Inhaled Foreign Body (Adult)


Aspiration of organic or inorganic material into the tracheobronchial tree.


  • At the laryngeal inlet: coughing, choking, hoarseness, or cyanosis

  • Below the cords: inspiratory stridor and coughing

  • In a bronchus: unilateral wheezing and coughing

  • If diagnosis is delayed, the patient may present with recurrent pneumonia, empyema, hemoptysis, or bronchopleural fistula.


Organic material (e.g., beans or other food products) may absorb fluid from surrounding structures and become engorged, causing complete airway obstruction. Inspissated oral secretions and/or mucous plugs may also lead to respiratory arrest through an obstructive mechanism. Inorganic material that does not cause a significant obstruction may be tolerated for years with minimal symptoms.

Differential Diagnosis

  • Pneumothorax

  • Bronchospasm

  • Tracheal injury

  • Airway compression from the intrathoracic mass

Immediate Management

  • In adults, foreign body aspiration is rarely a true emergency.

    • Monitor closely and give supplemental oxygen while the operating room is prepared.

    • The ability to convert from flexible to rigid bronchoscopy to thoracotomy should be immediately available.

  • Emergency foreign body asphyxiation usually involves material at the supraglottic larynx or subglottic trachea.

    • Direct laryngoscopy can be performed while the patient is awake and the foreign body is removed with Magill forceps.

    • Intubation with an ETT may be used to push the object into a distal bronchus, enabling life-saving ventilation while the patient is prepared for bronchoscopy.

Diagnostic Studies

  • Chest radiographs are useful only in patients with radio-opaque foreign bodies. Findings may include air trapping, atelectasis, pulmonary infiltrates, or mediastinal shift.

Subsequent Management

  • Rigid bronchoscopy is the most effective therapeutic intervention and usually requires general anesthesia.

    • Positive pressure ventilation can wedge the foreign body distally, creating a ball-valve obstruction.

    • Spontaneous ventilation using an inhaled anesthetic is the preferred technique. Spontaneous breathing enables ventilation when the bronchoscopist’s ocular window is open.

    • If neuromuscular blockade is needed to facilitate laryngoscopy, short-acting agents are preferred. Intermittent ventilation is possible through the bronchoscope. If positive pressure ventilation is necessary, consider an intravenous anesthetic technique to reduce operating room pollution with volatile agents.

  • Flexible bronchoscopy is the tool of choice when the foreign body is wedged in a distal segment, in patients with cervical spine pathology, or when the patient is intubated and mechanically ventilated.

    • Avoids general anesthesia and preserves spontaneous ventilation.

    • Preservation of the cough reflex is imperative in patients with a full stomach and also aids in foreign body expulsion. Use local anesthetics sparingly.

    • Sedatives should be administered judiciously.

    • A laryngeal mask airway may be inserted in an awake patient after topical anesthesia of the oropharynx, and can used as a conduit for the flexible bronchoscope. This provides some degree of airway control and is large enough to allow for extraction of the foreign body.

    • Special forceps and snares are passed through the working port of the bronchoscope. The bronchoscope, grasping device, and foreign body are all removed as a unit. If the object dislodges in the proximal trachea, place the patient into the Trendelenburg position, and ask him or her to cough.

    • If an endotracheal tube (ETT) is in place, the object may not pass through the ETT. In this case, it may be necessary to remove the endotracheal tube along with foreign body while being grasped under visualization through a bronchoscope.

Risk Factors

  • Advanced age

  • Neurologic disorders with impaired swallowing

  • Alcohol and sedative use

  • Trauma with loss of consciousness

  • General anesthesia

  • Seizures

Special Considerations

  • Massive hemoptysis may occur when the foreign body is removed. Consider lung isolation with a double-lumen ETT or bronchial blocker if bleeding cannot be controlled. Preparations should be made for thoracotomy or bronchial artery embolization.

  • Prolonged rigid bronchoscopy may lead to postoperative laryngeal edema. Treatment options include:

    • Nebulized racemic epinephrine

    • Helium/oxygen mixtures

    • Dexamethasone 10-mg IV bolus

  • Failed bronchoscopy may ultimately require thoracotomy and bronchotomy to remove the impacted object.

Further Reading

Rafanan AL, Mehta AC. Adult airway foreign body removal. What’s new? Clin Chest Med. 2001; 22(2): 319–330.Find this resource:

Swanson KL. Airway foreign bodies: what’s new? Semin Respir Crit Care Med. 2004; 25(4): 405–411.Find this resource:

Intrathoracic and Mediastinal Lesions Causing Tracheal, Bronchial, Cardiac, and/or Vascular Obstruction


Extrinsic or intrinsic obstruction of intrathoracic structures caused vby tumor, tracheal disease, or vascular compression, with potential to lead to cardiovascular collapse and/or the complete inability to oxygenate and ventilate.


  • Dyspnea

  • Cough

  • Orthopnea

  • Inspiratory stridor or expiratory wheeze

  • Hoarseness

  • Hemoptysis

  • Obstructive pneumonia


The common causes of obstruction include:

  • Malignancy

  • Primary airway tumors (usually intrinsic): squamous cell carcinoma, adenoid cystic carcinoma, or carcinoid tumor

  • Primary adjacent tumor (usually intrinsic): anterior or middle mediastinal tumors, lung carcinoma, or esophageal carcinoma

  • Metastatic cancer (extrinsic): renal, breast, colon, or sarcoma

  • Tracheal disease related to stenosis or tracheomalacia (intrinsic)

  • Vascular compression or ring (extrinsic)

General anesthesia can cause cessation of spontaneous ventilation, increased intrapleural pressure, and decreased functional residual capacity. As a result, airways that had been patent can collapse and cause worsening or complete obstruction.

Differential Diagnosis

  • Foreign body aspiration

  • Bronchospasm

  • Pneumothorax

Immediate Management


  • Identify the location of the lesion on imaging studies.

  • Identify the relationship of the lesion to adjacent structures.

  • Anticipate the potential for compression of the trachea, bronchi, and cardiovascular structures (>50% compression by tracheal lesions on imaging warrants a conservative approach).

  • Insert an intra-arterial catheter if there is a risk of cardiovascular compromise.

  • Obtain large-bore IV access. If superior vena cava (SVC) involvement or syndrome is suspected, insert a large-bore intravenous (IV) line in a lower extremity.

  • Ensure IV fluids can be administered rapidly.

  • Ensure that vasopressors are immediately available.

  • Equipment and personnel skilled in rigid bronchoscopy should be immediately available.

  • The surgical team must be present in the room.

  • Femoral arterial and venous access is established, with standby extracorporeal support device in cases in which the likelihood of an inability to ventilate is high (e.g., for large compressive lesions in a patient unable to lie flat without symptoms).

During the Procedure

  • A local anesthetic technique in the awake, spontaneously breathing patient is safest in patients with severe or potentially severe obstruction.

  • Avoid sedatives, or, if they are necessary, administer incrementally in small doses. Consider using short-acting drugs (e.g., propofol, remifentanil) or drugs that can easily be reversed.

  • Maintain the patient in the sitting position if possible.

  • Stepwise airway approach:

    • Awake fiberoptic examination of airway, trachea, and bronchi by anesthesia and surgical team to characterize the lesion and plan an approach to definitive airway management (may be facilitated by the use of a laryngeal mask airway—maintaining patient awake throughout—following topical local anesthesia)

    • Awake fiberoptic intubation with passage of tube distal to lesion if possible. If this is not possible, consider alternative strategies for securing the airway while maintaining spontaneous ventilation, including the use of extracorporeal support.

  • Securing the airway after induction should be attempted only with great caution, and with appropriately skilled individuals immediately available.


  • The airway is most safely managed prior to the induction of general anesthesia.

  • Gradually administer an inhalational agent or small doses of intravenous agents while maintaining spontaneous ventilation.

  • Attempt to assist with bag-ventilation

  • If successful

    • Overtake spontaneous ventilation with positive pressure.

    • Gradually increase the depth of anesthesia.

  • If not successful

    • Shifting the lesion by placing the patient in the lateral decubitus or prone position may improve ventilation.

    • Awaken the patient and reconsider the airway approach and/or using extracorporeal support.

  • If neuromuscular blockade is required, use a small dose of succinylcholine after the airway is secure and the ability to provide positive pressure ventilation has been confirmed. Neuromuscular blockade may cause the airway to collapse in a marginal patient. If succinylcholine is tolerated, longer-acting agents can be administered safely.

  • If the airway becomes completely obstructed, and is not relieved by repositioning the patient (lateral decubitus or prone position), attempt to pass a rigid bronchoscope or an armored endotracheal tube past the obstruction. An alternative rescue strategy is to pass a jet ventilator cannula distal to the lesion.

  • An intravenous anesthetic technique is preferable for maintenance, as inhalational agents will contaminate the operating room with surgical manipulation of the airway.

Diagnostic Studies

  • Neck and chest radiographs may demonstrate tracheal deviation, endoluminal narrowing, and obstructive pneumonia.

  • Computed tomography (CT) imaging of the neck and chest can determine the exact location, length, and nature of the obstruction.

  • Magnetic resonance imaging (MRI) and CT angiography are useful in characterizing vascular malformations.

  • Transthoracic echocardiography may be useful in evaluating the pericardium for malignant effusion or tumor.

  • Flow-volume loops are neither sensitive nor specific in characterizing obstruction.

Subsequent Management

  • Surgical airway resection and reconstruction

  • Tracheal (or bronchial) stent placement for symptomatic relief.

  • Awake tracheostomy with a long-length prosthesis allows for control of the airway distal to the lesion.

  • Endobronchial brachytherapy or external beam radiotherapy

  • Preoperative radiation can significantly reduce tumor burden.

  • Nd:YAG laser therapy in conjunction with rigid bronchoscopy can vaporize lesions and achieve hemostasis. Tracheal perforation, tracheal hemorrhage, and airway fire are risks with this procedure.

  • Photodynamic therapy

    • IV photosensitizer is administered and retained in tumor cells.

    • Specific wavelength light activates the agent and generates cytotoxic oxygen radicals.

Risk Factors

  • Prolonged intubation or tracheostomy may lead to stenosis or tracheomalacia.


Daily spontaneous breathing trials and sedation holidays may reduce the incidence of complications from prolonged intubation.

Special Considerations

  • There is a risk of acute intraoperative airway obstruction if the patient develops positional dyspnea while supine. If it may not be possible to maintain a patent airway during airway management or the surgical procedure, consider cannulating the femoral artery and vein to permit extracorporeal oxygenation and ventilation.

    • Superior vena cava syndrome is defined as obstruction of the SVC by tumor burden. These patients may have significant upper airway edema and friable tissue and require lower extremity IV access.

  • Postoperative airway obstruction may occur if manipulation causes tumor swelling.

    • Tracheal narrowing to <50% of normal confers a sevenfold increased risk.

Further Reading

Thompson A. Anterior mediastinal masses: look before you leap. Anesthes Anal. 2012; 114(2): 476; author reply 476–477.Find this resource:

Wood DE. Management of malignant tracheobronchial obstruction. Surg Clin North Am. 2002; 82(3): 621–642.Find this resource:

Major Hemorrhage during Mediastinoscopy


Bleeding during mediastinoscopy of >500 cc, or requiring exploration through a median sternotomy or thoracotomy. The incidence is 0%–0.4% in most large case series.


  • Arterial or venous surgical bleeding

  • Hypotension

  • Tachycardia

  • Cardiovascular collapse


The surgical approach for cervical mediastinoscopy involves passage between the trachea and paratracheal fascia with dissection and biopsy of lymph nodes in the superior mediastinum. This region contains a number of anatomic structures in addition to the trachea, including the recurrent laryngeal nerve, thoracic duct, and esophagus, as well as major vasculature such as the azygous vein, innominate artery and vein, pulmonary artery, SVC, and aorta. Injury to these structures is uncommon, but may occur during surgical exploration of the mediastinum.

Differential Diagnosis

  • Accidental biopsy of a vascular structure

  • Azygous vein injury

  • Innominate vein or artery injury

  • Pulmonary artery injury

  • Injury to the aortic arch

Immediate Management

  • Tamponade bleeding via surgical compression (packing wound with gauze soaked in dilute epinephrine, digital pressure, compression with mediastinoscope).

  • Establish large-bore IV access in the lower extremities if innominate vein injury is suspected.

  • Begin volume resuscitation.

  • Obtain cross-matched blood and set up rapid infusers.

  • Insert an intra-arterial catheter for invasive blood pressure monitoring.

  • Treat hypotension with ephedrine (5 mg IV) or phenylephrine (100 mcg IV) boluses. If refractory, consider phenylephrine infusion (0.5–1 mcg/kg/min).

Subsequent Management

  • Surgical exploration and repair is the definitive treatment for refractory bleeding. The surgical approach will depend on the injured vessel.

    • Midline sternotomy: Innominate vein or artery, pulmonary artery, anterior SVC

    • Right posterolateral thoracotomy: azygous vein, right pulmonary artery, posterior SVC, or bronchial artery

  • Lung isolation may enhance surgical exposure for right thoracotomy.

      Previously easy intubation and bleeding is easily controlled by the surgeon:

    • Confirm adequate neuromuscular blockade.

    • Change the ETT to a left-sided double-lumen tube (with or without an airway exchange catheter).

      Previously difficult intubation or uncontrolled bleeding:

    • Intubate the left mainstem by advancing the existing endotracheal tube over a fiberoptic bronchoscope.

    • Alternatively, insert a bronchial blocker into the right mainstem bronchus (see page [link]).

  • If definitive control at the bleeding source cannot be achieved despite a second incision for exposure, circulatory arrest with cardiopulmonary bypass may be required.

Risk Factors

  • Aberrant blood vessels

  • Superior vena cava (SVC) syndrome causing engorged vasculature

  • Mediastinal inflammation as a result of prior chemotherapy, radiation therapy, or surgical procedure


  • Surgical palpation of the lesion or needle aspiration before biopsy to identify a blood vessel.

  • Adequate neuromuscular blockade should be confirmed before biopsy to prevent movement during this critical period.

Special Considerations

  • Persistent hemodynamic instability with only minor apparent blood loss may be due to cardiac tamponade. For example, post-biopsy bleeding from the bronchial artery into the pericardial sac causing tamponade has been described. Transesophageal echocardiography should be performed to rule out pericardial effusion and tamponade physiology.

  • Patients who have had a prior sternotomy can present a particular challenge, especially if the vascular injury is at the level of the innominate vessels or the pulmonary artery. Prior sternotomy increases the risk for cardiac injury on repeat sternotomy; however, this must be weighed against the risk of uncontrolled bleeding from the injured vessel. The surgical team may consider a judicious upper hemisternotomy or resection.

Further Reading

Ahmed-Nusrath A, Annamanneni R, Wyatt R, Leverment J. Management of major hemorrhage during mediastinoscopy. J Cardiothorac Vasc Anesthes. 2006; 20(5): 762–763.Find this resource:

Lohser J, Donington JS, Mitchell JD, Brodsky JB, Raman J, Slinger P. Case 5—2005 Anesthetic management of major hemorrhage during mediastinoscopy. J Cardiothorac Vasc Anesthes. 2005; 19(5): 678–683.Find this resource:

Park BJ, Flores R, Downey RJ, Bains MS, Rusch VW. Management of major hemorrhage during mediastinoscopy. J Thorac Cardiovas Surg. 2003; 126(3): 726–731.Find this resource:

One-Lung Ventilation: Hypoxemia


Low PaO2 and low SaO2 in a patient who is receiving one-lung ventilation.


  • Low oxygen saturation by pulse oximetry

  • Dark arterial blood

  • Cyanotic patient

  • Cardiac dysrhythmias


Pathophysiology is multifactorial. A shunt develops in the nonventilated lung after residual oxygen is resorbed. In the ventilated lung, regions with a low ventilation to perfusion ratio (West zone III) develop as a result of atelectasis and from compression by the nonventilated lung, mediastinal structures, and the diaphragm. Other causes of hypoxemia from the ventilated lung include hypoxic pulmonary vasoconstriction (causing redistribution of blood to the nonventilated lung and increasing shunt), secretions, and double lumen tube or lung isolation device malposition.

Differential Diagnosis

  • Increased metabolic rate for oxygen

  • Decreased oxygen delivery (i.e., a low cardiac output state)

Immediate Management

  • Eliminate causes proximal to the double lumen tube, including disconnection and ventilator failure.

  • Mild hypoxemia (SpO2 >90%):

    • Increase FiO2 to 100%.

    • Examine the airway with a fiberoptic bronchoscope to ensure correct position of double lumen tube or lung isolation device.

    • Check the ventilated lung for obstruction or secretions—passage of suction catheter is more efficient than using the narrow port on fiberoptic bronchoscope.

    • Ensure adequate cardiac output and oxygen carrying capacity.

    • Recruit the ventilated lung. Follow with addition of PEEP if using low tidal volume ventilation (Note: This will only work if the lung is being ventilated in a noncompliant region on the low end of its pressure volume curve.)

    • Apply continuous positive airway pressure to nonventilated lung (start with 5 cm H2O to avoid distention of operative lung).

    • Consider switching to a total intravenous anesthetic technique. Hypoxic pulmonary vasoconstriction is impaired by potent volatile anesthetics.

    • Consider increasing tidal volume to 6–10 cc/kg.

  • If there is no improvement or the patient is severely hypoxic (SpO2 <90%):

    • Inform the surgeon and ventilate both lungs.

    • If there is no improvement, or the preceding steps are not possible, ask the surgeon to clamp the pulmonary artery if a pneumonectomy of nonventilated lung is planned.

    • If there is no improvement, consider high-frequency jet ventilation to the operative lung.

    • If there is no improvement, consider nitric oxide or almitrine (not available in the United States).

    • If no improvement, consider extracorporeal membrane oxygenation (ECMO).

Diagnostic Studies

  • Arterial and mixed venous blood gas measurement

  • Fiberoptic bronchoscopy

Risk Factors

  • Patients with increased or normal ventilation and perfusion to the operative lung will have a larger shunt during one-lung ventilation.

  • Right-sided operations (right lung normally receives 60% of blood flow)

  • Low PaO2 during two-lung ventilation

  • Normal or high FEV1/FVC ratio


  • Maintain two-lung ventilation as long as possible.

  • Ensure proper double lumen endotracheal tube or lung isolation device position after changing the patient’s position.

  • Ensure appropriate ventilator settings when beginning one-lung ventilation (in patients with normal lungs, pressure control ventilation, 4–6 cc/kg ideal body weight with 5–10 cm H2O PEEP, respiratory rate 10–15/min, FiO2 0.5–0.8).

  • Adapt ventilatory strategy to lung pathology.

  • Avoid using a high concentration of potent volatile anesthetic agents, which blunt hypoxic pulmonary vasoconstriction.

  • Avoid delivering a large tidal volume or high level of PEEP to the ventilated lung. This increases pulmonary vascular resistance and may shunt blood to the nonventilated lung.

Further Reading

Hartigan PM. Physiology of one-lung ventilation. In: Hartigan PM, ed. Practical manual of thoracic anesthesia. 1st ed. New York: Springer; 2010:71–92.Find this resource:

Karzai W, Schwarzkopf K. Hypoxemia during one-lung ventilation: prediction, prevention, and treatment. Anesthesiology. 2009; 110(6): 1402–1411.Find this resource:

Lohser J. Evidence-based management of one-lung ventilation. Anesthesiol Clin. 2008; 26(2): 241–272.Find this resource:

One-Lung Ventilation: Increased Airway Pressure


Increase in peak or plateau inspiratory airway pressure


  • Elevated airway pressures during volume-controlled mode of ventilation

  • Low tidal volume during a pressure-controlled mode of ventilation

  • Low blood pressure


The most common cause of elevated airway pressure during one-lung ventilation is malposition of the double lumen endotracheal tube or lung isolation device, which causes a larger volume of gas is displaced into a smaller portion of lung and increases pressures. Other causes include delivering an excessive tidal volume to one lung, secretions, bronchospasm, and tension pneumothorax.

Differential Diagnosis

  • Double lumen tube or lung isolation device malposition

  • Obstruction within a double lumen endotracheal tube (blood, secretions, foreign body)

  • Delivering an excessive tidal volume to one lung

  • Bronchospasm

  • Tension pneumothorax

  • Air trapping/auto-PEEP (allow patient to exhale fully)

Immediate Management

  • Inspect the ventilator tubing and endotracheal tube for kinks.

  • Disconnect the patient from the ventilator and allow to exhale fully to exclude air trapping/auto-PEEP.

  • Manually ventilate the patient to evaluate lung compliance.

  • If high airway pressure is accompanied by hypoxemia, resume two-lung ventilation.

  • Perform fiberoptic bronchoscopy to ensure proper positioning of double lumen tube or lung isolation device.

  • Pass a suction catheter through the lumen leading to the ventilated portion of the lung to eliminate obstruction.

  • Ensure delivery of appropriate tidal volume and PEEP settings for one-lung ventilation (in patients with normal lungs, pressure control ventilation, 4–6 cc/kg ideal body weight with 5–10 cm H2O PEEP, respiratory rate 10–15/min, FiO2 0.5–0.8).

  • Address other causes individually.

Risk Factors

  • Surgical manipulation of the airway

  • Change in patient position

  • Right-sided double lumen endotracheal tube: The right upper lobe orifice may become misaligned. This causes the entire tidal volume to be delivered to the right lower and middle lobes.

  • Obstructive lung disease is a risk factor for air trapping (use long expiratory times).


Confirm correct placement of the double lumen endotracheal tube or lung isolation device after changing the patient’s position or after significant surgical manipulation.

Further Reading

Hartigan PM. Physiology of one-lung ventilation. In: Hartigan PM, ed. Practical manual of thoracic anesthesia. 1st ed. New York: Springer; 2010:71–92.Find this resource:

Tension Pneumothorax


Abnormal presence of gas in the pleural cavity with inability to escape, causing pressure on intrathoracic structures.


  • High peak airway pressure

  • Decreased tidal volume

  • Decreased SpO2, SvO2

  • Hypotension

  • Tachycardia

  • Distension of neck veins

  • Subcutaneous emphysema

  • Contralateral tracheal deviation

  • Hyperresonance of the affected chest

  • Hyperexpansion of the affected chest

  • Reduced breath sounds in the affected chest

  • Compression of bronchi on fiberoptic inspection of affected side

  • Elevation of the mediastinum in the surgical field


Gas passes through the lungs and accumulates in the pleural space as a result of high airway pressure, rupturing of a bleb, or through the chest wall. A one-way valve effect prevents gas from escaping the pleural space. Increasing pressure in the pleural cavity from accumulation of gas results in clinical symptoms by compressing intrathoracic structures, including the mediastinum, lung, and blood vessels.

Differential Diagnosis

  • Hyperinflation of the ventilated lung with intrinsic PEEP (disconnect patient from ventilator circuit and allow exhalation)

  • Double lumen tube or lung isolation device malposition

  • Bronchospasm

  • Extrinsic lung compression

  • Hemothorax

  • Cardiac tamponade

Immediate Management

  • Inform surgical team.

  • Resume two-lung ventilation.

  • Increase FiO2 to 1.0.

  • Consult the surgeon about the ability to access the lung from the surgical field:

    • Ask the surgeons if they can dissect a plane to the affected pleural space between the aorta and esophagus posteriorly, and the pericardium anteriorly.

    • Accessing this space will immediately decompress the pneumothorax.

  • If the preceding steps are not possible, position the patient supine and decompress the affected side with a large-bore needle or a long 14-gauge IV catheter in the second intercostal space at the midclavicular line.

  • After the pneumothorax has been relieved, insert a chest tube.

  • If there is uncertainty about the diagnosis and the patient is hemodynamically stable, fiberoptic bronchoscopy may show compression of major bronchi and a chest radiograph will provide a definitive diagnosis.

Diagnostic Studies

  • Chest X-ray (in a hemodynamically stable patient) reveals midline shift to the contralateral side and a dark hemithorax on the affected side (due to lung collapse).

Subsequent Management

  • Tube thoracostomy

Risk Factors

  • Elevated peak airway pressures

  • Malposition of the double lumen endotracheal tube causing high airway pressure

  • Obstructive lung disease

  • Acute lung injury

  • Pleural blebs

  • Penetrating chest wall injury

  • Recent central venous catheter insertion


  • Adjust ventilator settings to avoid elevated airway pressure.

  • Ensure that a double lumen endotracheal tube or lung isolation device is correctly positioned.

Special Considerations

  • Tension pneumothorax has been reported during one-lung ventilation in the absence of the classic signs of hypoxemia and hypotension.

Further Reading

Bacon AK. Crisis management during anaesthesia: pneumothorax. Qual Saf Health Care. 2005; 14(3): e18–e18.Find this resource:

Finlayson GN, Chiang AB, Brodsky JB, Cannon WB. Intraoperative contralateral tension pneumothorax during pneumonectomy. Anesthes Analges. 2008; 106(1): 58–60.Find this resource:

Malik S, Shapiro WA, Jablons D, Katz JA. Contralateral tension pneumothorax during one-lung ventilation for lobectomy: diagnosis aided by fiberoptic bronchoscopy. Anesthes Analges. 2002; 95(3): 570–572, table of contents.Find this resource:

Tracheal Injury


Injury to any portion of the extrathoracic or intrathoracic trachea that may involve complete or partial disruption of the trachea. Mortality estimates vary widely depending upon the etiology.


  • Dyspnea

  • Hoarseness or stridor

  • Signs of external trauma

  • Subcutaneous emphysema

  • Pneumothorax, pneumomediastinum or pneumopericardium

  • Cyanosis and oxygen desaturation

  • Hemoptysis


  • Iatrogenic causes include endotracheal intubation, use of tube exchange catheter, percutaneous dilational tracheostomy, and cricothyroidotomy, which often causes tearing of the posterior membranous trachea.

  • Blunt trauma

    • Tracheal injury is frequently within 2 cm of the carina.

    • Chest trauma may cause complete transection or a posterior membranous tracheal tear.

    • Upper airway trauma may result in fractured laryngeal cartilages.

    • Flexion-extension injury may precipitate full laryngotracheal separation.

  • Penetrating trauma mostly occurs to the cervical trachea, but one-third may affect the larynx.

  • Mucosal tears are often self-limited, but through-and-through tears require surgical management.

Differential Diagnosis

  • Pneumothorax

  • Foreign body aspiration

  • Pulmonary hemorrhage

  • Bronchospasm

Immediate Management

Iatrogenic Injury

Iatrogenic trauma that results in small tears to the middle and upper third of the trachea may be managed conservatively.

  • Advance the tracheostomy or endotracheal tube beyond the lesion using a fiberoptic bronchoscope.

  • Inflate the cuff to eliminate airway pressure on the proximal tear.

  • Long-term ventilation may be required to allow healing.

Airway Management of Blunt or Penetrating Trauma

Airway manipulation may quickly turn a stable situation into a life-threatening one by precipitating complete obstruction.

  • General guidelines

    • Tracheostomy equipment and a skilled surgeon should be present.

    • Maintain spontaneous ventilation. Avoid intravenous sedatives and neuromuscular blockers until the airway is secure.

    • Positive pressure ventilation before a cuff has excluded the injury can worsen existing pneumothorax, pneumomediastinum, or air dissection around the airways.

    • Awake fiberoptic bronchoscopy is the diagnostic and interventional procedure of choice for determining the nature of the injury as well as securing the airway.

    • The goal is to inflate a cuffed airway device or cannula distal to tracheal disruption to permit positive pressure ventilation.

    • If 100% FiO2 is required to maintain oxygenation, advise the surgical team. Concomitant use of electrocautery may cause a fire.

  • Cervical tracheal and upper airway lesions

    • Patients with open tracheal disruptions may be oxygenated via facemask and cannulated with the aid of a bronchoscope. A jet ventilator cannula may also be used for oxygenation.

    • Rigid bronchoscopy may be diagnostic when blood in the airway precludes flexible bronchoscopy. An inhaled anesthetic technique with spontaneous ventilation can be used to facilitate this approach, but there is a possibility of aspiration of gastric contents. The clinical scenario should dictate the best anesthetic approach.

    • With blunt laryngeal injuries, attempted conventional laryngoscopy and endotracheal intubation may fracture the cricoid cartilage or provoke complete transection. Avoid cricoid pressure. Awake oral fiberoptic intubation or awake tracheostomy distal to the lesion are safe airway management options.

  • Lower tracheal lesions

    • Blunt chest trauma disrupts the trachea within several centimeters of the carina. Tracheostomy will not permit ventilation in this situation.

    • Flexible fiberoptic bronchoscopy is essential in diagnosing and safely crossing the lesion. Intubation is best achieved over the bronchoscope.

    • The ETT cuff should be placed distal to the lesion and proximal to the carina if possible. Alternatively, consider endobronchial intubation or jet ventilation through a catheter located distal to the lesion.

Diagnostic Studies

  • Do not delay airway management for diagnostic studies.

  • Radiographic findings may include cervical emphysema, pneumothorax, pneumomediastinum or air column disruption.

  • Computed tomography is sensitive, but the patient may not be able to lie flat. Sedatives may cause respiratory arrest and should be avoided until the airway is secure.

  • All patients with tracheal injury should undergo an esophagoscopy to rule out esophageal perforation.

Associated Pathology

  • Neurologic trauma including cervical spine and closed head injury

  • Related airway pathology

    • Maxillofacial trauma

    • Laryngotracheal hematoma and edema

    • Subcutaneous emphysema of upper airway and epiglottis

  • Esophageal injury

  • Vascular injury with associated hemodynamic instability

Subsequent Management

  • The approach for high lesions is a collar incision. The mediastinal trachea is repaired via a right posterolateral thoracotomy. The left approach is sometimes used, so the surgeon should be consulted.

  • One-lung ventilation may be required to facilitate surgical exposure via a thoracotomy approach.

  • An airway isolation device or blocker may be used.

  • Alternatively, bronchial intubation with a double lumen endotracheal tube may safely be achieved over a fiberoptic bronchoscope or airway exchange catheter of adequate length.

  • The endotracheal tube may need to be pulled back to facilitate visualization of the surgical anastomosis. An armored endotracheal tube and sterile circuit should be used to facilitate patient ventilation across the surgical field.

  • At the conclusion of surgery, bronchoscopy should be used to position the cuff of the ETT distal to the anastomosis.


Iatrogenic injury during endotracheal intubation can be minimized by ensuring that the tip of a stylet does not protrude past the tip of an ETT.

Special Considerations

  • If it is impossible to maintain a patent airway during instrumentation or other stages of the procedure, the femoral artery and vein should be cannulated to permit extracorporeal oxygenation and ventilation prior to proceeding.

  • Cricothyroid pressure (Sellick’s maneuver) is contraindicated if upper tracheal or laryngeal injury is suspected, because it can cause complete tracheal disruption.

Further Reading

Chu CP, Chen PP. Tracheobronchial injury secondary to blunt chest trauma: diagnosis and management. Anaesthes Int Care. 2002; 30(2): 145–152.Find this resource:

Schneider T, Storz K, Dienemann H, Hoffmann H. Management of iatrogenic tracheobronchial injuries: a retrospective analysis of 29 cases. Ann Thorac Surg. 2007; 83(6): 1960–1964.Find this resource:

Welter S. Repair of tracheobronchial injuries. Thorac Surg Clin. 2014; 24(1): 41–50.Find this resource: