Momen M. Wahidi
Ian J. Welsby
1. Therapeutic bronchoscopy is most commonly employed to treat patients with central airways obstruction due to malignant disease.
2. Rigid bronchoscopy provides definitive control of the airway permitting the use of general anesthesia to maximize patient comfort.
3. Patients can undergo bronchoscopy with transbronchial biopsy without stopping aspirin therapy, but clopidogrel should be stopped 5 days prior to the procedure.
4. As with any shared airway case, close communication between operator and anesthesiologist is vital for maximum patient safety.
The patient is a 47-year-old female with stage 4 adenocarcinoma involving the left lung. A prior stent was placed in the left mainstem bronchus due to tumor invasion of the proximal airway. Now, the tumor has invaded the stent to the point where complete airway obstruction is imminent. She is referred for stent exchange and tumor debulking.
She has a history of 100 pack-years of smoking but no other medical problems. She is oxygen dependent at home on 2L/min nasal cannula.
Medications are alprazolam and albuterol. Vital signs: BP 110/80, HR 82, room air SpO2 85%. Laboratory examination is notable only for a WBC of 11.5.
Therapeutic bronchoscopy, previously practiced primarily by thoracic surgeons, is becoming more commonly performed by pulmonologists who receive specialized training in the performance of airway surgical techniques for the treatment of central airways obstruction. Performing these procedures involves the use of the rigid bronchoscope, which requires careful coordination of care between the anesthesia team and the proceduralist. Several issues around the use of rigid bronchoscopy can often lead the anesthesiologist into unfamiliar territory, including release of the airway into the hands of the proceduralist, turning the head of the patient away from the anesthesiologist during the procedure, and often ceding control of ventilation to the procedural team. Good communication regarding procedural planning, ventilatory strategy, and anesthesia management are critical to optimize patient safety and provide for a successful procedure.
Therapeutic bronchoscopy is most commonly employed to treat patients with central airways obstruction (CAO) due to benign or malignant etiology. While the incidence of CAO is unknown, it is a commonly encountered clinical problem present in 20% to 30% of patients with primary lung cancer1 and 7% to 18% of patients post-lung transplantation.2 Additional common causes of CAO include tracheal stenosis, either post-tracheostomy or idiopathic, tracheomalacia, and foreign body aspiration.1 While many of the techniques that will be described in this section are amenable to use with the flexible bronchoscope, rigid bronchoscopy provides definitive control of the airway permitting the use of general anesthesia to maximize patient comfort (Table 11–1).3 In addition, the rigid bronchoscope becomes a conduit for use of a variety of tools and suction devices to perform minimally invasive airway surgery. The bronchoscope itself can become a therapeutic tool useful for dilation of airway stenoses, and “coring out” of airway tumor providing rapid relief of central airway obstruction.3
Table 11–1. Indications for Rigid Bronchoscopy
The rigid bronchoscope was the only method of bronchoscopy available from the advent of the bronchoscope in 1897 by Gustav Killian, until the introduction of the flexible fiberoptic scope in 1967 by Ikeda. After the introduction of flexible bronchoscopy, use of the rigid bronchoscope declined by pulmonologists in North America. Its distinct advantages in controlling the airway while facilitating the passage of a wide variety of tools for minimally invasive airway surgery in conjunction with the development of reliable stents to promote airway patency has led to a renewal in interest in the use of rigid bronchoscopy by the pulmonary community over the past 15 years.4
Rigid bronchoscopy can be used for any bronchoscopic indication, however, the additional requirements of general anesthesia generally result in most centers limiting its use to therapeutic indications such as relief of central airway obstruction, foreign body removal, and for investigation of massive hemoptysis.
Rigid bronchoscopy is generally well-tolerated among most patients, even those with significant respiratory disabilities due to their underlying pulmonary disease. However, several medical conditions may occur which raise the risk for complications. Major conditions to consider include ischemic or arrhythmic heart disease, bleeding diathesis (coagulopathy, thrombocytopenia, uremia), neurologic disease or head trauma, and respiratory insufficiency. Although bronchoscopy can be performed in patients who fall short of the ideal, the risk of the procedure increases accordingly, and options for more invasive manipulations (biopsies, lengthy procedures, etc) can be limited.
Preoperative laboratory studies, including platelet count, coagulation studies, blood urea nitrogen, and creatinine level, are often obtained to assess for bleeding tendencies. However, multiple studies examining the utility of preoperative laboratory examinations have determined that this is not universally necessary, but should be tailored to patients with medical histories suggesting an abnormality. In a retrospective study of 305 bronchoscopies with biopsy, Kozak and Brath identified five clinical risk factors which should prompt further pre-operative evaluation including prior anticoagulant therapy, liver disease, family or personal history of bleeding tendencies, active bleeding or recent transfusion requirements, and presence of an unreliable historian.5
Absolute contraindications to bronchoscopy are few and include inability to provide informed consent, status asthmaticus, severe hypoxemia, and unstable cardiovascular conditions. Detailed below are some of the main factors to consider when selecting a patient for bronchoscopy.
Although bronchoscopy can be safely performed in asthmatic patients, it is associated with a significant drop in FEV1 and PaO2 post-procedure. This drop correlates inversely with the concentration of methacholine required to produce a 20% fall in FEV1 at baseline but not with the usual measures of asthma severity such as albuterol use, symptom scoring, and peak flow variation.6 Therefore, bronchoscopy should be approached cautiously in the patient with asthma, and avoided entirely in the setting of status asthmaticus. Elective procedures should be deferred until bronchospasm is effectively controlled.
HEAD TRAUMA/ELEVATED INTRACRANIAL PRESSURE
Increased intracranial pressure (ICP) has been anecdotally cited as a relative contraindication to bronchoscopy because of concerns that the rise in intrathoracic pressure induced by bronchoscopy-associated cough could abruptly raise ICP and precipitate herniation. A retrospective study found no increase in neurologic complications in patients with space-occupying central nervous system lesions undergoing bronchoscopy, although pretreatment with steroids was recommended to decrease cerebral edema.7 More recently, a prospective study of 23 patients with intracranial drains in place revealed substantial, though transient, increases in ICP in patients undergoing bronchoscopy, despite adequate levels of sedation, analgesia, and paralysis.8 No acute deterioration in the patient’s clinical status was observed, but unfortunately, long-term complications or sequelae from these changes remain unknown.8 Therefore, although fiber-optic bronchoscopy is often necessary in the care of patients after neurologic events, it should be used with caution in this patient population.
HYPOXEMIA/HIGH OXYGEN REQUIREMENT
Bronchoscopy carries a higher risk in patients who are hypoxemic at baseline, although determining the cause of hypoxemia is a common indication for bronchoscopy. Unfortunately, hypoxemia is also a complication of bronchoscopy, resulting from sedation-related hypoventilation and ventilation-perfusion mismatch secondary to partial airway occlusion (from bronchoscope), atelectasis from frequent suctioning, airway bleeding, lavage fluid, and jet ventilation.9 While there is no absolute amount of supplemental oxygen that is a contraindication for bronchoscopy, caution should be used in patients with high oxygen requirements. Severe hypoxemia with PaO2 greater than 65 to 70 mm Hg despite supplemental oxygen therapy is generally considered a contraindication.10
Use of anticoagulant and antiplatelet agents is common among patients referred for bronchoscopy. Therefore, it is important to carefully review all medications with the patient prior to bronchoscopy and make appropriate recommendations for continuing or holding medications prior to the procedure date.
Aspirin Aspirin was previously considered a contraindication to bronchoscopy due to its anti-platelet effects and prolongation of bleeding time. However, a large multicenter randomized trial found no difference in bleeding from transbronchial biopsies in the aspirin compared with the no aspirin group.11 Therefore, it is generally accepted that patients can undergo bronchoscopy with transbronchial biopsy without holding aspirin therapy.
Clopidogrel In contrast to aspirin, clopidogrel significantly increases bleeding risks following transbronchial biopsy. When the effect of clopidogrel on the incidence of bleeding was studied during transbronchial biopsy, significant bleeding rates increased to 89% compared with 3.4% in the control group.12 In a small number of patients receiving both aspirin and clopidogrel, the incidence of significant bleeding was 100% following transbronchial biopsy.12 Given the relatively long half-life of clopidogrel, most practices require patients to discontinue clopidogrel a minimum of 5 days prior to undergoing bronchoscopy with transbronchial biopsy.
Thrombocytopenia There is little data regarding what threshold for platelets constitutes safe levels for bronchoscopy. Transfusion guidelines and expert statements have recommended minimum platelet counts of 20,000 to 50,000/mm3 for fiberoptic bronchoscopy and greater than 50,000/mm3 for transbronchial biopsy.13
Procedure Risks and Complications
The risks of bronchoscopy and anesthesia should be specifically reviewed with the patient. The risk of major complications from bronchoscopy, including pneumothorax, pulmonary hemorrhage, infection, and respiratory failure, is 0.6%. When transbronchial biopsy is performed, the risk of serious complications reaches 1% to 6%.14 Complications specifically related to rigid bronchoscopy include airway perforation, pneumomediastinum, and fatal hemorrhage due to injury of the great vessels, which are rare. Minor complications from bronchoscopy include fever, cough, bronchospasm, transient hypoxia, and hemoptysis. Additionally, cardiovascular complications can occur from the stress of the procedure itself, particularly in high risk patients. Cardiac events can include vasovagal reactions, arrhythmias, myocardial ischemia, angina, and cardiac arrest.15 The mortality rate from bronchoscopy is approximately 0.01%, and has decreased in recent years as monitoring capabilities and technology have improved.14
The rigid bronchoscope is essentially a stainless steel tube with a beveled tip at the distal end, while the proximal end usually contains a series of ports for ventilation, passage of suction catheters, grasping tools, a telescope, or a flexible bronchoscope (Figure 11–1). Fenestrated caps may be placed over the ports to permit closed ventilation during the procedure. Adult bronchoscopes are generally 9 to 13 mm in diameter and 40 cm long, while tracheoscopes are of similar diameter but are only 25 cm in length. Fenestrations are present in the side-wall at the distal end of the bronchoscope to allow for continued ventilation of the opposite lung if the scope is passed down one of the mainstem bronchi during the procedure.
Figure 11–1. Rigid bronchoscope and telescope. Note head portion of bronchoscope with ports for passage of tools and attachment to the anesthesia circuit or jet ventilator adaptor.
Prior to bronchoscope insertion, the patient must be adequately anesthetized. Many centers choose to administer a muscle relaxant as well, although this is not absolutely required. The patient’s neck is hyperextended, and with the fingers of the left hand, the upper lip and teeth are covered with the operators thumb, the index finger is inserted into the patient’s mouth to displace the tongue towards the left side of the mouth, and the middle finger is used to cover the lower lip and teeth to prevent injury of these structures. The bronchoscope is held in the right hand with the barrel of the scope resting between the thumb and first finger with the bevel of the distal end of the scope facing down. The tip of the scope is inserted into the patient’s mouth against the base of the tongue. The tongue is visualized via the telescope inserted through the bronchoscope, and the scope is advanced along the base of the tongue until the epiglottis is visualized. The bevel of the scope is advanced under the epiglottis, and the tip is rotated upward, using the thumb located over the patient’s upper mandible as a fulcrum to lift the epiglottis and bring the vocal cords into view. The scope is then rotated 90 degrees clockwise to allow the beveled tip to slide between the cords. Rotation is continued an additional 90 degrees as the bronchoscope enters the trachea to run the bevel against the posterior wall of the trachea to prevent injury to the membranous tracheal wall.3
ANESTHETIC MANAGEMENT FOR RIGID BRONCHOSCOPY
Due to the irritating nature of the rigid intubation, virtually all centers perform rigid bronchoscopy under general anesthesia. Standard American Society of Anesthesiologists’ recommended monitoring should be used for these cases. Additionally, a radial arterial line is generally useful for real-time hemodynamic monitoring and for providing access for arterial blood gas analysis as indicated.
The anesthesia plan can be based on a balanced technique with positive pressure ventilation or a spontaneously breathing technique. For spontaneous assisted ventilation,16 anesthesia is closely titrated to permit spontaneous ventilation. The rigid bronchoscope is capped and the mouth is packed with gauze to provide a seal around the barrel of the bronchoscope. Ventilation is provided by attaching the anesthesia circuit to the side port of the bronchoscope, resulting in a closed system that is suitable for delivery of oxygen and gas anesthetics to the patient if desired. Instruments are introduced into the airway through fenestrated caps on the rigid scope. The patient is lightly anesthetized for the majority of the procedure to permit continued spontaneous ventilation except during particularly noxious portions of the procedure when anesthetics are titrated up to prevent patient motion. At these times, ventilation may need to be supported with positive pressure ventilation, as the patient is likely to become apneic. While an effective technique, some operators find the need for capping the rigid bronchoscope cumbersome, because this limits the number of instruments that may be introduced into the bronchoscope. Also, in order to reduce entrainment of ambient air with subsequent dilution of inspired oxygen and anesthetic gas concentrations, high gas flows are required, which increases the consumption of inhaled anesthetics and pollutes the operating room environment.
Two basic approaches are currently practiced to provide positive pressure ventilation during rigid bronchoscopy. The most basic form uses intermittent apnea while the proceduralist performs the necessary procedures followed by capping of the rigid scope to allow intermittent positive pressure ventilation. This approach becomes quite cumbersome for longer or complex procedures and is not favored by most centers. Therefore, the majority of North American interventional pulmonologists use some form of jet ventilation during rigid bronchoscopy, either a Sander’s jet ventilator or an automated jet ventilator, which allows the anesthesiologist to be freed from managing the Sander’s jet during the procedure.17,18
Limited data exist comparing outcomes between ventilation strategies, however there is some evidence to suggest that spontaneous assisted ventilation may reduce rates of reintubation following rigid bronchoscopy.16 This result may be partially explained by the need for muscle relaxants with jet ventilation, underscoring the importance of monitoring and avoidance of residual curarization while using this technique. Positive pressure techniques in a paralyzed patient are better suited to the more complex procedures such as airway tumor debulking and customized stent deployment. Therefore, details of the anesthetic technique discussed below focus on this.
Induction of anesthesia is typically intravenous, as this patient population is susceptible to paroxysms of coughing. Standard considerations for rapid sequence induction apply and the choice of induction agent is at the anesthesiologist’s discretion, although propofol or ketamine are better suited to patients with preexisting bronchospasm. Procedures generally have a duration of 20 to 60 minutes, and choice of neuromuscular blocker should reflect this. Residual curarization or recurarization in this population will be poorly tolerated,16 so pancuronium is rarely indicated. A balanced technique is not mandatory but avoids the cardiovascular effects of deep anesthesia that would otherwise be necessary, as bucking or coughing against the rigid bronchoscope can lead to serious tracheal injury. Depending on the circumstance, the trachea can be intubated prior to the bronchoscopic procedure, or more usually induction will occur once the pulmonologist is poised to pass the rigid bronchoscope. The rigid bronchoscope is not cuffed and may not protect against aspiration, but the airway is continuously visualized and endobronchial toilet can be immediately performed should soiling occur.
The passage of the rigid bronchoscope is very stimulating and blunting of the pressor response to intubation can be achieved with short acting opiates such as remifentanil or alfentanil, as postoperative pain is minimal and opiate induced respiratory depression will be dangerous. If the bronchoscope is capped appropriately necessitating intermittent use of the lumen for the procedure, interrupted inhalational anesthesia may be used for maintenance of anesthesia, however, a total intravenous anesthetic (TIVA) technique may better suited to rigid bronchoscopy to ensure continuous anesthesia delivery and avoid interruptions to the procedure. The TIVA should be started at the time of induction through a dedicated intravenous cannula that can easily be inspected to confirm intravenous delivery, especially if hemodynamic parameters or anesthesia depth monitors suggest inadequate anesthesia.
Assuming TIVA is used for maintenance of anesthesia, jet ventilation is used as described below, with either a jet ventilator or manually delivered using a Sanders injector. Adequate tidal volume is estimated by visually appreciating chest rise and is greatly facilitated by reverse Trendelenburg positioning. Arterial blood gas analysis or use of a percutaneous carbon dioxide monitor is advisable to avoid over or under ventilation. Prior to emergence, the patient is intubated with a cuffed endotracheal tube, reexpansion of previously collapsed lung segments is achieved with positive end expiratory pressure, and a final toilet bronchoscopy is performed with a flexible bronchoscope. Full reversal of neuromuscular blockade is confirmed prior to extubation.
This patient population is at high risk for respiratory distress after extubation and consideration should be given to nebulized bronchodilators or lidocaine for bronchospasm or excessive coughing respectively. The team should have a low threshold for awake bronchoscopy to diagnose and treat excessive secretions mobilized from newly expanded lung segments, de novo airway bleeding or stent migration.
Jet ventilation employs a short burst of high-pressure gas delivered through a narrow (often 1-3 mm in diameter) catheter to provide ventilation through an open, uncuffed airway. Tidal volumes are usually low, often significantly less than dead space, with respiratory rates ranging from 60 to 150 breaths per minute. Given the low tidal volumes produced by the jet ventilator, mechanisms other than conventional bulk flow become important for effective gas exchange during jet ventilation.
Five mechanisms have been described to explain gas transport with jet ventilation: (1) Bulk flow or convective gas transport is responsible for gas delivery during conventional mechanical ventilation and likely plays a role in the large airways during jet ventilation as well. (2) Coaxial flow describes movement of gas in one direction down the center of an airway while movement in the opposite direction occurs along the airway periphery. This mechanism is very dependent on airway geometry and occurs more frequently at the site of bifurcations. (3) Taylor dispersion is a complex phenomenon that describes gas dispersion along the front of bulk gas flow. This probably plays the greatest role within the larger airways. (4) Molecular diffusion occurs at the alveolar level and plays a significant role in gas mixing within the alveoli in both jet and conventional ventilation. (5) Pendelluft describes the intra-alveolar mixing of gas due to impedance differences. This phenomenon may also involve airway gas as well and so result in alveolar ventilation.19
Other important considerations when using jet ventilation include the site of the injection catheter placement. We generally place the injection catheter at the proximal end of the bronchoscope (Figure 11–2). Others move it deeper into the airway to reduce dead space ventilation. This technique requires continuous airway pressure monitoring to prevent barotrauma, as airway obstruction related to the introduction of instrumentation through the bronchoscope may result in elevations in airway pressure.20 In addition, caution must be used when central airways obstruction is present as placement of the catheter distal to an airway lesion may result in a ball valve mechanism leading to elevated alveolar pressures and pneumothorax.
Figure 11–2. Components needed for jet ventilation through the bronchoscope (Sanders injector). Wall connector for oxygen supply, reducing valve and pressure gauge, high-pressure tubing, toggle switch, and needle injector jet. (From: Eisenkraft JB, Neustein SM. Problems in Anesthesia. Vol 4. Philadelphia: JB Lippincott, 1990:223, with permission.)
There was some concern that ball valve induced barotrauma could also occur with ventilation proximal to sites of central airway obstruction. This question was addressed by Biro et al who used a balloon inflated to different diameters in the large airways during jet ventilation proximal to the site of obstruction and measured airway pressures proximal and distal to the site of obstruction. They found that while peak airway pressures rose at the proximal position, distally there was no change in peak pressures, but expiratory pressures rose closer to peak pressures. Since peak pressures were thought to be at a safe level, concerns of elevating airway pressures distal to a central airways stenosis were not substantiated.21
Determination of ventilation parameters during jet ventilation can be challenging. The variables that may be changed are frequency, inspiratory time, and inspiratory pressure. Tidal volumes are generally unknown during jet ventilation, but are titrated to the lowest pressure capable of producing a slight chest rise. Increasing respiratory rates may be used to elevate mean airway pressures and enhance oxygenation. Caution should be used when setting I:E ratios greater than 1:2 to permit adequate time for exhalation and to prevent gas trapping.22 Our practice is to check an arterial blood gas early in the procedure to ensure adequate ventilation, while monitoring oxygenation continuously via a pulse oximeter. When available, use of transcutaneous CO2 monitoring may be useful in assessing ventilation.
Patients with significant tracheal stenosis can prove difficult to ventilate by jet ventilation with an automated system. This situation may be addressed by performing initial attempts to open the airway using an endotracheal tube and a flexible bronchoscope. Alternatively, manual jet ventilation may provide breath-to-breath adjustment in jet duration to produce chest rise as the obstruction is addressed with conversion to automated ventilation once the initial obstruction has been relieved. Finally, determination of absolute inspired FiO2 is difficult as gas entrainment of room air is an unpredictable but significant portion of the delivered breath. Consequently, the set FiO2 and the actual FiO2 may be very different. Use of additional O2 delivered via a catheter into the rigid bronchoscope may prove useful in elevating delivered O2 in patients who prove difficult to oxygenate.
COMPLICATIONS OF JET VENTILATION
Few studies are available detailing complications associated with jet ventilation, specifically with rigid bronchoscopy. Fernandez-Bustamante et al described their experience with 316 patients undergoing rigid bronchoscopy for interventional procedures. Complications were present in 40% of patients. The most common complications were hypercapnea, hypoxemia, and hemodynamic instability. These complications were transient and did not result in an increase in hospital stay. Serious complications included post-anesthesia laryngospasm in 2 patients, pneumothorax in 1 patient and 3 peri-operative deaths related to inability to open an obstructed airway.23
In a national survey of the United Kingdom otolaryngologists using high-pressure source ventilation (automated high-frequency jet ventilation and manual jet ventilation), use of manual jet ventilation was associated with greater number of complications including 3 critical care admissions and 3 deaths. Use of high-frequency jet ventilation was associated with 2 critical care admissions and no deaths. However, only 17% of study sites used high-frequency jet ventilation.24
Central airway obstruction may result from benign or malignant conditions. Benign conditions include tracheal stenosis secondary to endotracheal intubation or following tracheostomy, due to tracheomalacia from disorders such as relapsing polychondritis, Wegener granulomatosis, stenosis at anastomic sites following lung transplantation, and secondary to human papilloma virus infections of the airway.1 Virtually any type of malignancy can involve the airways, but the most common types are lung cancer, breast cancer, and renal cell carcinoma. Airway obstruction may take one of three forms; extrinsic compression, endobronchial obstruction, and mixed types composed of elements of both endoluminal obstruction and extrinsic compression.25 Identification of the type of obstruction is important because it helps the physician determine the best course of treatment for relief of central airway obstruction, or if a procedure is likely to be effective.
A variety of therapeutic procedures are available to relieve airway obstruction due to malignancy or benign airway stenosis (Table 11–2). Rapid relief of airway obstruction may be obtained using heat therapy such as endobronchial laser, electrocautery, or argon plasma coagulation (APC).
Table 11–2. Currently Available Bronchoscopic Ablative Therapies
Light amplification of stimulated emission of radiation (Laser) was first described for use in the airway in 1976,26 and is used in many centers as the primary tool for rapid resection of central airway tumors. Several types of laser are available for use in the airway, with each type having advantages and disadvantages regarding ability to produce coagulation, vaporization, and with differing depth of tissue penetration depending on wavelength of light emitted and absorption and scattering of light energy by the tissues of the airway. The most commonly used laser is the neodymium-yttrium aluminum garnet (Nd-YAG) device, with a wavelength of 1064 nm that results in excellent coagulation and vaporization of tissues. The treatment may be applied via a flexible catheter placed through the rigid bronchoscope or via the working channel of a flexible bronchoscope. This allows for devitalization of tumor tissue followed by removal with forceps to open the airway.25
Other commonly used lasers include the CO2 laser favored by ENT surgeons for work on the upper airway. This laser is a cutting laser, and has limited coagulation ability. In addition depth of tissue penetration is more superficial compared with the Nd-YAG laser due to the high degree of absorption of light energy by water in tissues at 1060 nm, which is the CO2 laser light’s wavelength. Until recently, CO2 lasers were cumbersome to use in the lower airway because the laser light could not be conducted in flexible catheters. However, the recent release of a flexible light guide may increase the use of this device among interventional pulmonologists. The potassium–titanyl-phosphate (5-KTP) laser emits a wavelength of 532 nm with good absorption by vascular structures, and thus is good for treating vascular lesions such as angiomas.27 The yttrium aluminium pevroskite:neodymium YAP-Nd laser wavelength of 1340 nm produces a moderately good coagulation effect but has questionable vaporization ability. This laser has otherwise similar operating characteristics as the Nd-YAG system.27
The principles of safe use of lasers for tumor debulking from the airway were described by Dumon et al in 1984. They emphasized application of laser light along the long axis of the airway to minimize chance of perforation through the airway wall. The laser itself is applied for brief time periods, less than 1 second intervals at modest power settings, with the primary goal of producing tissue coagulation followed by manual removal of desiccated tissue. Control of depth of penetration may be achieved by moving the laser delivery fiber between 0.3 and 1 cm from the tumor tissue. The catheter is moved closer to achieve tissue vaporization or more distant for a coagulative effect.28 Using this technique, 70% of central airway obstructions are relieved.25
In the case of significant hemorrhage, the laser is applied circumferentially around the center of the bleeding to achieve hemostasis, terminating the coagulation at the center of the bleeding site. Oxygenation must remain a priority during any airway procedure, although care must be taken when using any form of heat therapy in the airway. The inspired FiO2 should be reduced to 40% or less to avoid ignition of flammable components within the airway. Should a patient begin to desaturate, use of the laser must be stopped, FiO2 must be increased and the airways inspected for possible collections of blood or mucous in the lower airways. The rigid bronchoscope may need to be advanced into the airway to bypass the obstructing tumor while the airway debris is removed. Once adequate oxygenation is restored, tumor debridement may be continued.28
The most concerning complications during use of laser therapy are perforation of a major vessel and perforation of the airway and pneumomediastinum. With cautious application of the laser along the axis of the airway, and particular care when treating tumors along the membranous posterior portion of the trachea, significant complication rates are less than 1% in most large series that have been reported.25
Although the use of lasers for airway debridement remains popular, the technique has significant drawbacks. Primarily, expensive equipment is required. The equipment may be cumbersome to move due to large size, although many of the newer devices are more portable. Adequate eye protection must be worn by all personnel in the operating theatre to prevent ocular injury, which may be uncomfortable to some providers. Finally, use of reflective devices in the airway must be avoided when possible to prevent inadvertent scattering of the laser beams and injury to the patient or proceduralist.
Although airway laser remains the most popular technique for management of CAO due to tumor, a similar effect can be obtained using pulsed electrical field and an electrocautery probe extended through the rigid or flexible bronchoscope. In this case the tissue is devitalized using direct contact, permitting excellent control of tissue destruction. The electrocautery is fired in short bursts with frequent observation of the underlying tissue injury to avoid unwanted extension of the coagulation effect. Similar to laser therapy, devitalized tissue may then be removed with the use of grasping forceps with a minimum of bleeding1,4 (Figure 11–3). There have been no direct comparisons of laser therapy and electrocautery for the relief of central airways obstruction, however reported efficacy has been similar with both techniques. Similar precautions to those used during laser debridement must be observed, particularly when treating tumors adherent to or arising from the airway wall. Electrocautery has an advantage in that it requires less investment in equipment and does not require the use of special eye protection or the avoidance of reflective surfaces during its use. The primary disadvantage with use of electrocautery is that the probe tip may become fouled with tissue debris during repeated use requiring intermittent cleaning during the procedure.
Figure 11–3. Debridement of an anaplastic large cell carcinoma. Upper left: A large polypoid mass is extending from the right upper lobe into the trachea. The lumen of the left mainstem bronchus can be seen distal to the mass. Upper right: Application of electrocautery to coagulate the proximal portion of the mass allowing safe debridement. Lower left: Application of a cautery snare to remove large portions of the tumor. The forceps are used to stabilize the piece of tissue once it has been freed from the main mass and prevent it from migrating to the left mainstem bronchus producing an obstruction of the uninvolved lung. Lower right: View from the trachea showing the right mainstem bronchus after debridement of the mass. The right upper lobe is entirely occluded with tumor, but the remaining airways of the right lung are patent.
Argon Plasma Coagulation
An additional technique that uses heat therapy is argon plasma coagulation (APC). This technique employs argon gas which, when exposed to high voltage becomes ionized (plasma) and conducts electricity to underlying tissue, resulting in a superficial coagulation effect. APC is a noncontact technique, in that the electrical energy is carried by the gas to the underlying tissue, and so this technique may be used to deliver energy around corners and is difficult to reach locations in the airway. The effect of APC is more superficial than either laser or electrocautery, causing coagulation to a depth of 2 to 3 mm within the airway.29 This limited penetration provides the ability to “spray” the coagulation effect within the airway making APC a useful tool for control of airway bleeding and devitalization of granulation tissue (Figure 11–4). The superficial coagulation effect also makes APC extremely safe resulting in lower rates of complications such as airway perforation and massive hemorrhage,30 although there are theoretical concerns for the development of gas embolism with higher flow rates and longer pulse duration with the use of APC.31
Figure 11–4. Argon plasma coagulation used to treat the base of a resected carcinoid tumor to prevent additional bleeding.
Special comment should be made on the concern for airway fire during the use of heat-based therapy. Airway fire has been well-recognized as a potential complication during the use of laser treatment of the airways. Risks for the development of airway fire include inspired oxygen levels greater than 40%, longer duration of treatment, increased power application, and application of heat near a combustible element such as a flexible bronchoscope or plastic endotracheal tube.32 To reduce the risk of airway fire the FiO2 must be reduced to 0.40 or less prior to the application of a heat based therapy. It is our practice to use the minimal amount of O2 tolerated during these procedures. Only rarely will we use heat-based treatments with the FiO2 greater than 0.30. Furthermore, power settings should be reduced to the minimum levels necessary to achieve effect in order to avoid excessive heating within the airway. Should an airway fire ensue, it is critical to remove the burning elements including the endotracheal tube immediately to avoid thermal injury to the airway, as well as injury from smoke inhalation.
Treatment of airway stenosis following tracheostomy or lung transplantation may be performed using inflatable balloons or rigid dilators to disrupt the fibrous connective tissue that forms at the site of the prior airway injury.33 Often, a combination of techniques such as use of an electrocautery knife to cut the membranous region of a stenosis followed by dilation with an inflatable balloon and removal of granulation tissue with forceps is required to achieve the desired result. Finally, the rigid bronchoscope itself can be used as a therapeutic instrument to “core out” central airway tumors after adequate desiccation and coagulation have been performed using laser therapy or electrocautery.25
THERAPIES WITH DELAYED EFFECT
In addition to the rapidly acting procedures above, there are several therapies that provide delayed effect in debulking airway malignancies. Cryotherapy is a safe and effective method that uses nitrous oxide gas to cool the tip of a metal probe placed through the working channel of the flexible bronchoscope. Once the gas flow is activated, the tip of the catheter rapidly cools to induce freezing of tissues at the point of contact and a small margin of surrounding tissue. The tissue thaws and the cycle may be repeated. The freeze-thawing of tissues results in delayed necrosis and sloughing of the treated area over the next several days.34 This technique has been shown to be effective in tumor debulking and improving central airways obstruction. Cryotherapy is also useful for removal of foreign bodies.35 The tip of the probe is placed on the foreign body, and the gas flow is activated resulting in the foreign body being frozen to the catheter tip. The foreign body is then removed from the patient by removing the flexible bronchoscope with the catheter still in the working channel without turning off the gas flow.
Additional delayed efficacy treatments include photodynamic therapy, which employs a systemically administered photosensitizing agent prior to the procedure that is preferentially concentrated by tumor cells. Photophrin is currently the only sensitizing agent licensed for use in the United States. When stimulated by light of 630 nm via an argon/dye or diode laser applied through a light guide, oxygen radicals are produced in tissues, which have concentrated the previously administered medication, resulting in tissue necrosis.36 Often necrosis is so exuberant that a repeat procedure is needed in 24 to 48 hours after light administration to debride necrotic tumor that can cause airway obstruction. Efficacy is good in patients with central airways tumors where up to 70% report improvement in symptoms ofdyspnea.33 Primary complications include severe sunburn due to the photosensitizing effect of the medication which may last as long as 6 weeks, and bleeding due to the destruction of vascular tumor.37
Finally, brachytherapy is a palliative technique that employs locally delivered radionuclide for treatment of endobronchial tumor resulting in central airway obstruction. The advantages of this approach are: delivery of high-dose radiation directly to the tumor tissue with limited penetration to surrounding tissue due to the rapid drop off of radiation dose with distance from the source, ability to modify the area of treatment to conform to the shape of the tumor, and ability to precisely target the tissue of interest.37 The radionuclide most commonly used is iridium-192 delivered in an encapsulated form via a polyethylene catheter inserted via the working channel of the flexible bronchoscope. The catheter is placed adjacent to the area to be treated and the bronchoscope removed. The catheter is then secured at the nose or mouth, and the position is confirmed using fluoroscopy. The iridium source is then afterloaded into the catheter and dwells for a period of time until the desired dose is delivered, generally 7 Gy for high-dose applications, and the catheter and source removed from the patient. Efficacy for symptom palliation ranges from 65% to 95%.38-40 A recent Cochrane review examined efficacy between external beam radiation therapy and high-dose endobronchial therapy and showed no difference between the two treatments.41 Complications are rare, although fatal hemoptysis is reported in 2% to 11% of treated patients.40
Types of stents
Modern airway stenting began as a modification of the Montgomery T-tube, with silicone stents popularized by Dumon in the late 1980s.42 Shortly afterwards, the self-expandable metal stent was developed and became widely used due to its ease of deployment without the need for rigid bronchoscopy as is required for silicone stent placement.43 More recently, hybrid metal-silicone stents have been developed which share some of the advantages and disadvantages of each type of stent.
Silicone stents are composed of silicone sleeves fitted with external studs to retard stent migration in the airway (Figure 11–5). The stent wall is relatively thick at 2 mm and so significant portions of the airway lumen may be occupied in smaller (<10 mm outer diameter) stents. Stents are sized from 10 to 20 mm in outer diameter and in lengths ranging from 2 to 8 cm. In addition, Y-shaped stents are available for placement at the main carina with limbs of the Y extending proximally into the trachea and distally into each of the mainstem bronchi. The limbs of the Y are not symmetrically angled, but instead are more acute for the left mainstem bronchus take-off to accommodate the positioning of the two mainstem bronchi.
Figure 11–5. Proximal (upper) and distal (lower) views of a left mainstem silicone stent.
Rigid bronchoscopy is required for silicone stent placement. During deployment, the stent is rolled along the long axis and placed into a steel delivery tube sized the same length as the rigid bronchoscope (Figure 11–6). The bronchoscope is advanced to the mid-point of the desired airway obstruction and the deployment tube is inserted into the bronchoscope. The stent is then pushed forward using a pushrod placed down the deployment tube, followed by removal of both the pushrod and deployment tube. The rigid scope is then withdrawn while holding the incompletely expanded stent in place until the proximal end is free from the bronchoscope. Generally, the stent will fully expand, but occasionally it may need to be opened using a dilation balloon. If the stent has been positioned distal to the area of narrowing, it may be dragged proximally using large forceps, however, stents that have been placed too proximally cannot be advanced, and must be removed and reinserted.
Figure 11–6. Stent deployer for Dumon style silicone stents. The deployer consists of a tube that has the stent inserted into it and a pushrod. A silicone stent can be seen partially deployed at the end of the insertion rod.
SELF-EXPANDING METAL STENTS
Self-expanding metallic stents were introduced in the mid-1990s as an alternative to silicone stents. The majority of these stents are constructed of nitinol, an alloy composed of nickel and titanium. This metal has the properties of being flexible while retaining excellent shape memory and so can be compressed onto a factory packaged deployment rod that will expand to its initial diameter after it is deployed. These stents are less likely to migrate than silicone stents44 as they rapidly embed into the surrounding mucosa. They are also less likely to become occluded with secretions, because the open meshwork of the stent allows normal ciliary function of the underlying mucosa to move secretions into the upper airway. However, lumen occlusion with granulation tissue or recurrent tumor can be a significant problem with these stents. In addition, once metallic stents are placed they are rapidly incorporated into the airway wall making removal very difficult.45 Over time, stress fractures often develop in the stents resulting in loose wires, which may migrate through the airway wall causing injury to the surrounding lung and mediastinal structures. Because of these complications, the American College of Chest Physicians and the FDA have recently issued warnings against the use of metallic airway stents for benign airway diseases.46
An advantage of metal stents over silicone stents is the ability to be placed without the need for rigid bronchoscopy, but rather using a flexible bronchoscope and fluoroscopic guidance. To achieve this, the patient is examined with a flexible bronchoscope under moderate sedation. The obstructed airway of interest is identified, the lesion is measured using the bronchoscope, and a guidewire is passed through the working channel of the bronchoscope across the area of stenosis. Next, the bronchoscope is positioned at the distal and proximal ends of the stenosis, and surface markers are placed on the patient’s chest under fluoroscopy. The bronchoscope is removed with the guidewire left in place. The self-expandable metal stent is then passed over the guidewire, positioned in the airway between the previously placed surface markers and deployed under fluoroscopy to ensure accurate positioning.
Hybrid silicone and nitinol stents have recently been developed which share some of the characteristics of silicone and metallic stents. These stents are constructed of a polyurethane or silicone sleeve with supporting nitinol struts. They share many of the advantages of metal stents in that they are self-expanding and so may be deployed across a tight stenosis and act to open the lesion via the radial force exerted by the wire mesh (Figure 11–7). The silicone sleeve prevents tumor in-growth through the stent, and also prevents the stent from granulating into the airway wall. This enhances patency as well as allows for removal of the stent at a later time if needed.
Figure 11–7. Left mainstem anastomosis stenosis in a patient after bilateral orthotopic lung transplantation. (Upper) View of the left anastomosis from the proximal left main-stem bronchus showing a 75% occlusion of the airway. (Middle) Distal view through the hybrid metal-silicone stent showing the upper and lower lobe orifices. (Lower) Proximal view of the left mainstem stent from the main carina.
One disadvantage of these stents has recently been recognized related to the open nature of the nitinol struts. These struts may fold inward on themselves during vigorous coughing or breathing. Generally they will re-expand to their original dimensions, but occasionally they remain collapsed. Case reports exist describing severe shortness of breath associated with collapsed tracheal stents requiring urgent removal.47 Due to this complication, we avoid placing these stents in the trachea when an alternative type of stent is available.
Efficacy and Complications of Stent Placement
Stents are generally effective in improving airway patency,48 and are associated with increases in FEV1.49 There are no randomized trials evaluating stent efficacy, survival benefit, or head-to-head comparisons of efficacy between types of stent. In addition, optimal placement of airway stents may be more complicated than previously perceived. Miyazawa et al examined flow-limiting segments of malignant airway stenosis in 64 patients using ultrathin bronchoscopy, flow volume loops, and 3-dimensional computed tomography reconstruction before and after central airways stenting. They found that the flow limiting segment migrated distally in 15% of patients after stent placement requiring additional airway stent deployment to optimize respiratory function.50 Significant complications are common and are as high as 50% in some series. Common complications include stent migration and occlusion by secretions, occasionally with significant airway obstruction requiring emergent procedures to clear the impacted secretions.
Choice of therapeutic approach is based on a variety of variables including the patient’s degree of dyspnea, location of tumor, whether the tumor is primarily endobronchial, or if the airway obstruction is secondary to extrinsic compression, equipment availability, and the level of local experience with the various techniques.
Our approach is initially to attempt to restore airway patency using a heat-based treatment in combination with manual debridement. Stent placement is usually reserved for the treatment of some component of extrinsic compression, although it is common to encounter CAO due to mixed intrinsic and extrinsic airway disease. The optimal use of airway stents in the setting of successfully resected intrinsic tumor is still controversial and requires further study. Generally speaking, the rapid effect of heat based therapies may have a less durable effect in the absence of additional treatment such as airway stenting, palliative radiation, or chemotherapy. Treatments such as photodynamic therapy or brachytherapy may delay the recurrence of tumor, and so may result in a longer lasting tumor reduction. Currently, there is no data available comparing efficacy between techniques. There is no demonstrated increase in life expectancy with the use of any of the above treatments, but substantial data exist suggesting efficacy in providing symptomatic relief.51-55
The objective of this section is to provide examples of our approach to a variety of situations and to highlight the need for a multimodality approach to central airways disorders.
The patient is a 36-year-old female diagnosed with refractory asthma with progressive shortness of breath for over 2 years. A CT scan of the chest shows significant obstruction of the mid-trachea extending to both mainstem bronchi. Minimal diameter of the trachea is 7 mm. Due to the difficulties in providing adequate oxygenation using jet ventilation in patients with high-grade tracheal stenoses, the initial ventilation strategy employed a large laryngeal mask airway to provide ventilation. A flexible bronchoscope was placed through the LMA and electrocautery was used to perform initial desiccation of the airway tumor. Close attention was paid to aspirating any blood or mucous released into the airway during this process to prevent obstruction of the narrowed airway.
Once the tracheal lumen was enlarged enough to allow for adequate ventilation via the jet ventilator, the rigid bronchoscope was inserted. Additional electrocautery was performed at the trachea and bilateral mainstem bronchi followed by “coring out” of the tumor using the barrel of the rigid bronchoscope to further enlarge the distal trachea and mainstem bronchi to near normal diameter. Additional tumor was removed with manual debridement using large forceps through the barrel of the rigid bronchoscope. At this point the airways were adequately debulked. There was a component of extrinsic compression that warranted further treatment via deployment of self-expandable metal stents. In this case covered stents were deployed at the left and right mainstem to prevent reocclusion of the airway by tumor. Finally, to maintain patency of the trachea, a silicone stent was deployed at the distal trachea just above the takeoff of the mainstem bronchi. While the stent was in place at the termination of the procedure, it ultimately migrated proximally within the airway due to the cone shaped distal trachea secondary to distortion of the anatomy by tumor. We elected not to place a self-expanding metal stent in this area because the terminal 0.5 cm of these stents is uncovered to allow anchoring in the airway. This would allow for tumor infiltration of the stent and may cause recurrent airway obstruction in the future. A hybrid stent was not placed due to concerns for buckling of the stent resulting in airway obstruction.
The patient was diagnosed with adenoid cystic carcinoma of the central airways and initiated chemotherapy and radiotherapy with stabilization of her airway disease and has had normal respiratory function for 2 years following her diagnosis.
The patient is a 68-year-old female who underwent a bilateral orthotopic lung transplant for treatment of endstage idiopathic pulmonary fibrosis. Her initial postoperative course was uncomplicated with the exception of mild rejection in the first postoperative month that was successfully treated with corticosteroids. Four months following transplantation her FEV1 had declined to 0.83 liters from a posttransplantation peak of 1.51 liters. On bronchoscopy she was noted to have stenosis of her right mainstem anastomosis that was occluding 75% of the lumen diameter. This was treated with balloon dilation bronchoplasty using a 3 cm by 12 mm in diameter balloon. This resulted in improvement of her FEV1 to 1.04 liters. Two months later, her FEV1 had declined again to 0.93 liters and she was noted to have recurrent right mainstem stenosis on flexible bronchoscopy. She underwent rigid bronchoscopy with repeat bronchoplasty. The lesion was complex, composed of a relatively large right mainstem bronchus that substantially narrowed to a relatively small bronchus intermedius.
Post-transplant bronchial stenosis is present in up to 15% of patients. The etiology of these lesions is not entirely understood, but ischemia of the bronchial wall is thought to play an important role in the development of airway stenosis. These lesions often require airway stenting to stabilize the stenotic site. The ideal stent for treatment of stenoses at the anastomosis site should be covered to prevent in-growth and occlusion of the stent by granulation tissue, and should be removable as it is thought that the stenotic lesions will remodel over time permitting removal of the stent and avoiding complications of a foreign body in the airway. We prefer to place silicone stents in these situations for the reasons stated above.
The rapid tapering of the airway from the mainstem bronchus to the bronchus intermedius prevented the use of a conventional silicone stent, because use of a stent large enough to fit snugly in the mainstem bronchus would be too large to anchor in the bronchus intermedius. Placement of a stent in the mainstem bronchus alone would be too short distal to the stenosis and would likely migrate into the proximal airway. To overcome these obstacles we selected a tapering silicone stent with a 10 mm outer diameter distal portion and a 12 mm outer diameter proximal portion. In addition, because this stent was going to cover the orifice of the right upper lobe, we cut a window in the stent corresponding to the location of the right upper lobe to permit ventilation of that airway. Following stent placement the patient’s FEV1 increased to 1.48 liters. The patient had no complications related to the stent and it was successfully removed 5 months following placement. The underlying stenosis appeared to have remodeled, and her FEV1 post-stent removal was 1.99 liters.
Case 3—Clinical Vignette
Considering the patient presented at the beginning of the chapter, two management decisions are required at the time of the procedure. The first relates to re-establishing airway patency. In the setting of prior endobronchial tumor, we can assume that some type of covered stent was initially deployed. This will limit our ability to provide heat-based therapy due to increased risk of airway fire or damage to a metal stent. Both lasers and electrocautery have been shown to increase risk of damage to metal stents resulting in wire breakage and loss of stent integrity. Argon plasma coagulation may be used safely in the presence of metallic stents, although stents covered with silicone or plastic coatings are still at risk for ignition. If the stent currently placed is covered metal, it has likely been infiltrated by the tumor at the uncovered ends and may prove extremely difficult to remove. In this case we would use judicious APC in combination with manual debridement to remove the obstructing mass. If a silicone or hybrid stent had been placed it may be possible to remove it, treat the underlying tumor bed, and replace the stent once adequate debridement had taken place.
The second decision would revolve around which consolidative therapy to employ in order to provide a more durable suppression of the airway tumor and maximize the palliative benefit of the procedure. In this case, consultation with the patient’s oncologist and radiation oncologist will be important. If different chemotherapies are still available, a systemic therapy would be a good first choice to suppress further tumor growth. If the patient has not received maximal radiotherapy, application of external beam radiation or brachytherapy for local treatment may be viable options. If no additional chemotherapy or radiotherapy is available, we would advocate the use of photodynamic treatment for devitalization of the local tumor bed to provide a longer symptom free interval for the patient.
Therapeutic bronchoscopy may be employed for treatment of a variety of benign and malignant airway conditions. These procedures require good communication between the anesthesia and procedural teams to ensure patient safety and a satisfactory outcome for these often critically ill patients. Rigid bronchoscopic procedures often pose unusual ventilatory challenges, and a good working knowledge of different ventilator strategies, in combination with flexibility in anesthetic management is necessary for all parties involved with these procedures.
1. Ernst A, Feller-Kopman D, Becker H, Mehta A. Central airway obstruction. Am J Respir Crit Care. 2004;169:1278-1297.
2. Santacruz J, Mehta A. Airway complications and management after lung transplantation. Proc Am Thorac Soc. 2009;6:79-93.
3. Beamis J. Modern use of rigid bronchoscopy. In: Bollinger C, Mathur PN, eds. Interventional Bronchoscopy. Basel, Switzerland: S Karger; 2000.
4. Wahidi M, Herth F, Ernst A. State of the art: interventional pulmonology. Chest. 2007;131:261-274.
5. Kozak E, Brath L. Do “screening” coagulation tests predict bleeding in patients undergoing fiberoptic bronchoscopy with biopsy? Chest. 1994;106(3):703-705.
6. Djukanovic R, Wilson J, Lai C, Holgate S, Howarth P. The safety aspects of fiberoptic bronchoscopy, bronchoalveolar lavage, and endobronchial biopsy in asthma. Am Rev Respir Dis. 1991;143(4 Pt 1):772-777.
7. Bajwa M, Henein S, Kamholz S. Fiberoptic bronchoscopy in the presence of space-occupying intracranial lesions. Chest. 1993;104(1):101-103.
8. Kerwin A, Croce M, Timmons S, Maxwell R, Malhotra A, Fabian T. Effects of fiberoptic bronchoscopy on intracranial pressure in patients with brain injury: a prospective clinical study. J Trauma. 2000;48(5):878-882.
9. Wahidi MM, Rocha AT, Hollingsworth JW, Govert JA, Feller-Kopman D, Ernst A. Contraindications and safety of transbronchial lung biopsy via flexible bronchoscopy. A survey of pulmonologists and review of the literature. Respiration. 2005;72(3):285-295.
10. Zavala D. Pulmonary hemorrhage in fiberoptic transbronchial biopsy. Chest. 1976;70(5):585-588.
11. Herth F, Becker H, Ernst A. Aspirin does not increase bleeding complications after transbronchial biopsy. Chest. 2002;122(4):1461-1464.
12. Ernst A, Eberhardt R, Wahidi M, Becker H, Herth F. Effect of routine clopidogrel use on bleeding complications after transbronchial biopsy in humans. Chest. 2006;129(3):734-737.
13. Rebulla P. Platelet transfusion trigger in difficult patients. Transfus Clin Biol. 2001;8(3):249-254.
14. Pue C, Pacht E. Complications of fiberoptic bronchoscopy at a university hospital. Chest. 1995;107(2):430-432.
15. Matot I, Kramer M, Glantz L, Drenger B, Cotev S. Myocardial ischemia in sedated patients undergoing fiberoptic bronchoscopy. Chest. 1997;112(6):1454-1458.
16. Perrin G, Colt H, Martin C, Mak M, Dumon J, Gouin F. Safety of interventional rigid bronchoscopy using intravenous anesthesia and spontaneous assisted ventilation. A prospective study. Chest. 1992;102(5):1526-1530.
17. Conacher I. Anaesthesia and tracheobronchial stenting for central airway obstruction in adults. Brit J Anaesthesia. 2003;90(3):367-374.
18. Godden D, Willey R, Fergusson R, Wright D, Compton G, Grant I. Rigid bronchoscopy under intravenous general anesthesia with oxygen venturi ventilation. Thorax. 1987;37(7):532-534.
19. Chang H. Mechanisms of gas transport during ventilation by high frequency oscillation. J Appl Physiol Respir Environ Exercise Physiol. 1984;56(3):553-563.
20. Unzueta M, Casas I, Merten A, Landeira J. Endobronchial high-frequency jet ventilation for endobronchial laser surgery: an alternative approach. Anesth Analg. 2003;96(1):298-300.
21. Biro P, Layer M, Becker H, et al. Influence of airway-occluding instruments on airway pressure during jet ventilation for rigid bronchoscopy. Br J Anaesth. 2000;85(3):462-465.
22. MacIntyre NR. High-frequency ventilation. In: MacIntyre NR, Branson RD, eds. Mechanical Ventilation. Philadelphia, PA: WB Saunders Co; 2001.
23. Fernandez-Bustamante A, Ibanez V, Alfara J, et al. High-frequency jet ventilation in interventional bronchoscopy: factors with predictive value on high-frequency jet ventilation complications. J Clin Anesth. 2006;18(5):349-356.
24. Cook T, Alexander R. Major complications during anaesthesia for elective laryngeal surgery in the UK: a national survey of the use of high-pressure source ventilation. Br J Anaesth. 2008;101(2):266-272.
25. Bollinger C, Sutedja T, Strausz J, Freitag L. Therapeutic bronchoscopy with immediate effect: laser, electrocautery, argon plasma coagulation and stents. Eur Respir J. 2006;27(6):1258-1271.
26. Laforet E, Berger R, Vaughan C. Carcinoma obstructing the trachea. Treatment by laser resection. N Engl J Med. 1976;294(17):941.
27. Diaz-Jimenez J, Rodriquez A, eds. Laser Bronchoscopy for Malignant Disease: CRC Press; 2004. Beamis J, Mathur P, Mehta A, eds. Interventional Pulmonary Medicine: Lung Biology in Health and Disease; No. 189.
28. Dumon J, Shapshay S, Bourcereau J, et al. Principles for safety in application of neodymium-YAG laser in bronchology. Chest. 1984;86(2):163-168.
29. Keller C, Hinerman R, Singh A, Alvarez F. The use of endoscopic argon plasma coagulation in airway complications after solid organ transplantation. Chest. 2001;119(6):1968-1975.
30. Morice R, Ece T, Ece F, Keus L. Endobronchial argon plasma coagulation for treatment of hemoptysis and neoplastic airway obstruction. Chest. 2001;119(3):781-787.
31. Feller-Kopman D, Lukanich J, Shapira G, et al. Gas flow during bronchoscopic ablation therapy causes gas emboli to the heart: a comparative animal study. Chest. 2008;133(4):892-896.
32. Casey K, Fairfax W, Smith S, Dixon J. Intratracheal fire ignited by the Nd-YAG laser during treatment of tracheal stenosis. Chest. 1983;84(3):295-296.
33. Vergnon J, Huber R, Moghissi K. Place of cryotherapy, brachytherapy and photodynamic therapy in therapeutic bronchoscopy of lung cancers. Eur Respir J. 2006;28(1):200-218.
34. Ferretti G, Jouvan F, Thony F, Pison C, Coulomb M. Benign noninflammatory bronchial stenosis: treatment with ballon dilation. Radiology. 1995;196(3):831-834.
35. Reddy A, Govert J, Sporn T, Wahidi M. Broncholith removal using cryotherapy during flexible bronchoscopy. Chest. 2007;132(5):1661-1663.
36. Mang TS. Lasers and light sources for PDT: past, present, and future. Photodiagnosis Photodyn Ther. 2004;1:43-48.
37. Lee P, Kupeli E, Mehta A. Therapeutic bronchoscopy in lung cancer. Clin Chest Med. 2002;23(1):241-256.
38. Spratling L, Speiser B. Endoscopic brachytherapy. Chest Surg Clin N Am. 1996;6(2):293-304.
39. Huber R, Fischer R, Hautmann H, et al. Palliative endobronchial brachytherapy for central lung tumors: a prospective randomized comparison of two fractionation schedules. Chest. 1995;107(2):463-470.
40. Ozkok S, Karakoyun-Celik O, Goksel T, et al. High dose rate endobronchial brachytherapy in the management of lung cancer: response and toxicity evaluation in 158 patients. Lung Cancer. 2008;62(3):326-333.
41. Zorrilla AC, Reveiz L, Ospina E, Yepes A. Palliative endobronchial brachytherapy for non-small cell lung cancer. Cochrane Database Syst Rev. 2008;2:CD004284.
42. Dumon J. A dedicated trachobronchial stent. Chest. 1990;97(2):328-332.
43. Freitag L. Tracheobronchial stents. In: Bollinger C, Mathur P, eds. Interventional Bronchoscopy. Vol 30. Basel: Karger; 2000:171-186.
44. Chan A, Juarez M, Allen R, Albertson T. Do airway metallic stents for benign lesions confer too costly a benefit? BMC Pulm Med. 2008;8:7-15.
45. Lunn W, Feller-Kopman D, Wahidi M, Ashiku S, Thurer R, Ernst A. Endoscopic removal of metallic airway stents. Chest. 2005;127(6):2106-2112.
46. Lund W, Force S. Airway stenting for patients with benign airway disease and the Food and Drug Administration advisory: a call for restraint. Chest. 2007;132(4):1107-1108.
47. Trisolini R, Paioli D, Fornario V, Agli L, Grosso D, Patelli M. Collapse of a new type of self-expanding metallic tracheal stent. Monaldi Arch Chest Dis. 2006;65(1):56-58.
48. Dumon J, Cavaliere S, Diaz-Jimenez J, et al. Seven-year experience with the Dumon prosthesis. J Bronchol. 1996;3:6-10.
49. Vergnon J, Costes F, Bayon M, Emonot A. Efficacy of tracheal and bronchial stent placement on respiratory functional tests. Chest. 1995;107(3):741-746.
50. Miyazawa T, Miyazu Y, Iwamoto Y, et al. Stenting at the flow-limiting segment in tracheobronchial stenosis due to lung cancer. Am J Respir Crit Care. 2004;169(10):1096-1102.
51. Wood D, Liu Y, Vallieres E, Karmy-Jones R, Mulligan M. Airway stenting for malignant and benign tracheobronchial stenosis. Ann Thorac Surg. 2003;76(1):167-172.
52. Saad C, Murthy S, Krizmanich G, Mehta A. Self-expandable metallic airway stents and flexible bronchoscopy: long-term outcomes analysis. Chest. 2003;124(5):1993-1999.
53. Dasgupta A, Dolmatch B, Abi-Saleh W, Mathur P, Mehta A. Self-expandable metallic airway stent insertion employing flexible bronchoscopy: preliminary results. Chest. 1998;114(1):106-109.
54. Bollinger C, Probst R, Tschopp K, Soler M, Perruchoud A. Silicone stents in the management of inoperable trachobronchial stenosis: indications and limitations. Chest. 1993;104(6):1653-1659.
55. Lemaire A, Burfeind W, Toloza E, et al. Outcomes of tracheobronchial stents in patients with malignant airway disease. Ann Thorac Surg. 2005;80(2):434-438.